Analysis Of SCI-B-VAC's Overwhelming Phase III Clinical Data Suggests VBI Vaccines' Share Price Is Materially Undervalued
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Reference ID:
Genome-wide rare variant analysis for thousands of phenotypes in over 70,000 exomes from two cohorts
Description of included datasets
We used two cohorts in this analysis (Table 1). The first cohort was the set of sequenced UKB exomes. The UKB participants are between the ages of 40 and 69, and each has been extensively phenotyped, including consenting to making their medical records available. As described previously, the exome-sequenced set of UKB samples is enriched for individuals with MRI data, enhanced baseline measurements, hospital episode statistics, and linked primary care records (described for Category 170 at http://biobank.ctsu.ox.ac.uk/crystal/label.cgi?id=170). Of the 49,960 exome-sequenced individuals, 55% are female, and 40,468 are classified by the UKB as genetically of European ancestry (field 22006).
The second cohort included the exomes of 21,866 participants from the HNP (Table 1). These are unselected patients from Northern Nevada (Renown Health, Reno, Nevada) who consented to research involving their electronic medical records15. The participants in this cohort are aged 18–89+, and 68% are female. We classified 17,238 of these as European ancestry using principal component analysis based on 184,445 representative common variants (see “Methods”).
Collapsing rare variants
We performed a gene-based collapsing analysis to identify genes in which rare variants were, in aggregate, associated with a phenotype. In brief, we identified qualifying variants that met specific annotation criteria (see “Methods”) and had a MAF < 0.1%. We explored two gene-based collapsing models: (1) all non-benign coding and (2) only loss of function (LoF). The LoF model was used to identify associations where only putative LoF variants had an effect. In the coding model, we included 1,074,012 qualifying variants across 16,341 genes in the UKB cohort and 754,459 variants across 17,023 genes in the HNP cohort (see “Methods”). In the LoF model, we included 165,480 qualifying variants across 15,276 genes in the UKB cohort and 111,735 variants across 14,848 genes in the HNP cohort. There were 15,999 coding model genes and 13,474 LoF model genes that overlapped between the two cohorts. The median number of qualifying coding and LoF variants per gene in the UKB European ancestry population was 34 and six, and 22 coding and four LoF for the HNP cohort, respectively (Fig. 2 and Supplementary Fig. 1). When looking at all ethnicities, these numbers rose to 48 coding and seven LoF for the UKB cohort and 30 coding and seven LoF for the HNP cohort. The median percentage of people carrying qualifying variants in each gene was the same for both the UKB and HNP cohorts, both in European ancestry and across ethnicities: 0.13% for the coding model, and 0.02% for the LoF model.
Fig. 2: Histogram of number of qualifying variants per gene in European UKB cohort.
a Number of qualifying coding variants per gene. Eleven genes with >500 variants were excluded from plot. The median of variants per gene is 34 (range [1:2833]). b Number of qualifying coding variants per coding nucleotide of each gene. Sixteen genes with values >0.2 were excluded from the plot. The median of variants per nucleotide is 0.027 (range [0.0001:0.991]). c Number of qualifying loss of function (LoF) variants per gene. Six genes with >50 variants were excluded from plot. The median of variants per gene is six (range [1:178]). d Number of qualifying LoF variants per coding nucleotide of each gene. Nine genes with values >0.05 were excluded from the plot. The median of variants per nucleotide is 0.005 (range [9.5 × 10−5:0.25]). Plots for all ancestries and HNP cohort can be found in Supplementary Fig. 1.
Reducing test statistic inflation
We performed our main analysis in the European ancestry individuals, including related individuals, using a linear mixed model (LMM) to account for relatedness and population structure (see QQ plots in Supplementary Fig. 2). To reduce test statistic inflation for binary traits, genes were only included in the LMM analysis if the expected number of variant carriers in the case group was at least ten, based on the overall carrier and phenotype frequency21. This is an essential step to avoid false positive associations in gene-based collapsing analysis results, especially when there is a case-control imbalance (Fig. 3). This cutoff is for an individual to be carrying any qualifying variant in the gene, and thus it may reflect a situation where ten people are each carrying their own unique variants in a gene, with each variant only being seen once. This criterium does have the consequence of reducing the number of genes that can be investigated, as genes with low numbers of variants will not pass the threshold for all analyzed phenotypes. To compensate and permit coverage of these genes, we performed a supplementary Fisher’s exact test analysis of the binary traits that was restricted to unrelated European ancestry individuals. The Fisher’s exact test did not require a minimum number of carriers and showed no test statistic inflation (see Fig. 3 and Supplementary Fig. 2). For quantitative traits, we set a minimum threshold of five variant carriers (again, of any qualifying variant in that gene) to avoid overinterpreting signals coming from very small numbers of carriers.
Fig. 3: Overlaid QQ plots for the coding model with the phenotype atrial fibrillation.
This phenotype has a 1:22 case:control ratio. Shown are the results for a linear mixed model (LMM) meta-analysis of all European ancestry individuals with no minimum number of variant carriers required (black), with at least ten case carriers observed (red), and with at least ten case carriers expected in the case group based on the overall frequency (cyan), as well as a Fisher’s exact test (FET) of unrelated European ancestry individuals and all genes included (blue). The second to last condition is the requirement we set for our main analysis results. The one significant association is TTN, known from previous studies to be involved in phenotypes related to atrial fibrillation28. This association is significant (meta-analysis p < 3.4 × 10−10) in the LMM analysis, but it is difficult to distinguish from test statistic inflation without using the 10 expected case carriers cutoff (cyan). There is no inflation in the Fisher’s exact test of unrelated individuals, but this association is not significant in that analysis.
Gene-based collapsing meta-analysis
We analyzed 4264 phenotypes in the currently available European ancestry UKB exome cohort (Table 1, see Supplementary Data 1 for list of phenotypes). The corresponding QQ plots showed a general lack of test statistic inflation (see Supplementary Fig. 2). We then performed the same analyses in the 1934 phenotypes available from the European ancestry individuals in the HNP cohort, which was sequenced at Helix using the Exome+ assay15. We next performed a meta-analysis of the results from the two separately analyzed cohorts to identify statistically significant associations with the 1821 phenotypes that had been collected in both cohorts. We identified 47 significant associations (meta-analysis p < 3.4 × 10−10) (Table 2, Supplementary Data 2).
Table 2 Statistically significant associations from the European ancestry analysis. Incidence of independent replication
In addition to the meta-analysis, we wanted to clarify how often associations that were statistically significant in the UKB cohort alone would replicate in the independent HNP cohort. The success rate would inform our confidence in associations for phenotypes that were only measured in one cohort and not the other. We therefore also analyzed the European ancestry UKB data as the discovery cohort, with the HNP data as the replication cohort. By this method, we identified 39 associations that were statistically significant (LMM p < 3.4 × 10−10) in the discovery cohort, including 32 of the 47 associations from the meta-analysis and seven that were not significant in the meta-analysis. In the replication cohort, all 39 discovery phenotype/gene combinations showed directions of effect in that were consistent with the discovery signal, 32 (82%) achieved nominal significance (LMM p < 0.05), and 18 (46%) achieved statistically significant replication (LMM p < 0.001, the Bonferroni threshold for 39 tests). Given that the sample size was much lower in the replication cohort, it is not unexpected that some of the discovery associations did not achieve formal replication significance.
Analysis of phenotypes unique to each cohort
The high rate of replication of signals identified in the discovery cohort is encouraging for identifying significant associations for the 2556 phenotypes that could not be incorporated into the meta-analysis: 2443 phenotypes that were measured only in the UKB cohort and 113 that were only in the HNP cohort. This cohort-specific analysis identified 30 additional statistically significant associations, all from the UKB cohort (Table 2, Supplementary Data 2).
Analysis including all ancestries
Because we used an LMM, which can account for ancestry differences between individuals, we additionally performed an analysis that included all ancestries. The resulting QQ plots showed a general lack of test statistic inflation (see Supplementary Fig. 2). Of the 77 significant European ancestry associations described above, 64 (83%) generated a lower p value when the additional ancestries were added to the European subset, by a median of 3.4 orders of magnitude. In contrast, for the 17% of associations where the p value increased, it was only by a median of 0.6 orders of magnitude. Given the controlled test statistic inflation for these analyses, analyzing ancestries together in these datasets appears to be a reasonable method to boost power for discovery.
We therefore identified associations that were only significant in the mixed ancestry analysis. We identified 17 from the meta-analysis across cohorts and seven more from the analysis of phenotypes available in only one cohort (Table 3 and Supplementary Data 2). In addition, we found that each of the associations that were statistically significant in the mixed population also generated p values below 1 × 10–5 in the European ancestry subset (with the exception of some associations of HBB against various blood phenotypes, as this gene had very few European ancestry variant carriers in the UKB cohort). These associations were therefore already strong in the European ancestry subset but appeared to need a larger sample size to push them to significance.
Table 3 Statistically significant associations from the mixed ancestry analysis. Summary of gene-based results
The vast majority of the significant gene-phenotype associations identified were consistent with the current knowledge in the field (see Supplementary Data 2 for details). For example, rare variants in PCSK9 and APOB were associated with low density lipoprotein (LDL) levels, and rare LoF variants in TUBB1 were associated with platelet count.
We also found several associations that could be reasonably expected given current knowledge in the field but had not been previously identified in this type of population. For example, we found that rare coding variants in GP1BB were associated with higher mean platelet volumes in the general population, consistent with their previous association with some familial bleeding and platelet disorders22. As another example, we identified associations between rare coding variants in TYRP1 and blonde hair. A variant in this gene had previously been shown to cause blonde hair in dark-skinned individuals of Melanesian ancestry from the Solomon Islands, but until now it was thought that this gene did not play a role in blonde hair in other ancestries23,24.
Additional discoveries were novel. For example, we found that rare coding variants in STAB1 were associated with median T2star MRI measures in several brain structures, with the strongest association in the putamen. As STAB1 is a transmembrane receptor that is thought to play a role in angiogenesis, this finding provides novel hypotheses for further study. We also found an association of loss-of-function variants in SMAD6 with eye measurements. SMAD6 is a member of the SMAD family of signal transducers, inhibitors of BMP signalling. While its suggested role in human eye development is novel, BMP signalling pathways are involved in many human development processes (reviewed in ref. 25), including eye development, and a recent study found that the SMAD6 mouse homologue, Smad6, is essential for blood vessel function in the developing mouse retina22.
In addition to the associations that met our stringent significance criteria, there were a number of additional associations that are worth mentioning. There were multiple associations that generated significant p values in the meta-analysis but did not meet our criteria of having a better p value in the meta-analysis than in each individual cohort. For example, we observed a significant association between albumin levels and variants in the gene that encodes albumin, ALB (meta-analysis p = 7.3 × 10−19), but the meta-analysis p value was higher than the UKB-specific p value because there was only one carrier in the HNP cohort. In addition, we identified a novel association between LoF variants in the PAPPA gene and decreased height (p = 1.7 × 10−10 in the meta-analysis of unrelated individuals), but there were only two carriers in the HNP cohort and the p value rose above significance in the main LMM analysis that included relatives. While this gene has been previously implicated in GWAS of height, this is the first time that rare variants in this gene have been found to be significantly associated with height in a human population26,27. As one more example, our meta-analysis identified as significant (p = 2.5 × 10−20) the known association between LoF variants in TTN and the ICD10 code I48 for dilated cardiomyopathy28. However, there were only three expected case carriers, which failed our LMM threshold, and the Fisher’s exact test of unrelated individuals was just shy of significant (p = 6.9 × 10−10). Nonetheless, our main LMM analysis did identify an association between this gene and the related ICD10 code I42 for atrial fibrillation, a more common phenotype that included more expected variant carriers and thus passed our criteria (Table 2, Fig. 3).
Individual variant analysis
Mapping the precise effects of each contributing variant can elucidate the underlying biology of an association. We therefore performed association analyses of each individual rare variant to show the effects they had on the overall signal for each associated gene. For example, variants in SLC2A9 are associated with low urate levels (Fig. 4a, b). The protein encoded by this gene reabsorbs urate in the proximal tubules of the kidneys. Variants that disrupt the transmembrane regions or lower gene expression are known to be associated with hypouricemia29. We find that the association signal in this gene is most heavily concentrated in missense variants in the transmembrane regions of the protein, especially in the first half of the protein (Fig. 4a, b). Of the >40 variants associated with decreased urate levels, 88% are in or directly adjacent to a predicted transmembrane region (p < 0.05 from a Fisher’s exact test comparing the proportion of positively-associated missense variants in or adjacent to this domain compared with outside of this domain).
Fig. 4: Distribution of effects of rare variants in select genes in the UKB cohort.
a SLC2A9 protein and urate levels. The legend shows the gene, its associated phenotype, and the effect size (beta). The effect size is computed from the gene-based collapsing model, in which individuals were coded as either having or not having a qualifying variant. A positive value indicates that variant carriers have, on average, higher values for the phenotype, while a negative value indicates that variant carriers have lower values. The amino acid positions are shown on the x-axis, with the PFAM domain highlighted. The y-axis displays the beta of each individual variant, with negative values shown below and positive values above the horizontal axis. Variants are indicated according to their consequence as shown and labelled according to their amino acid change or splice site variation. The number inside the circle is the number of people carrying that variant. Darker lines connecting the variants to the gene and darker-filled shapes indicate more significant p values for the association. b Membrane topology plot of SLC2A9 showing variants with positive effect size (green) on urate levels and variants with negative effect size (pink). SLC2A9 (Glut9) reabsorbs urate in the proximal tubules of the kidneys. Variants that disrupt the transmembrane regions or lower gene expression are known to be associated with hypouricemia29. Here, 88% of the variants with negative betas, associated with lowered urate levels, are in or directly adjacent to a predicted transmembrane region, as opposed to only 55% of the variants with positive effect size. c GFI1B protein and mean platelet volume. Consistent with the literature, variants in the zinc finger domains are associated with increased platelet volumes, but we make the observation that some variants in between zinc fingers 3 and 4 may be having an effect in the opposite direction30,31. d ASGR1 protein and alkaline phosphatase levels. In addition to the known effects of LoF variants, we show that missense variants are also playing a role32. Plots of the other significantly associated genes are included in Supplementary Fig. 3.
Likewise, variants in different portions of GFI1B have distinct effects on mean platelet volume (Fig. 4c). Consistent with the literature, variants in the zinc finger domains of this gene are associated with increased platelet volumes (p < 0.05 from a Fisher’s exact test comparing the proportion of positively-associated missense variants in zinc fingers to outside of zinc fingers), but we make the observation that some variants between zinc fingers 3 and 4 may have an effect in the opposite direction (p < 0.05 from a Fisher’s exact test comparing the proportion of negatively-associated missense variants in this region to outside of this region, even after excluding all zinc finger variants)30,31.
In one more example, a significant association is observed between variants in ASGR1 and alkaline phosphatase AP levels. Previously, two LoF variants in this gene were found to be associated with AP levels, coronary artery disease, and non-HDL cholesterol32. In our analysis, the association is most strongly influenced by LoF variants, but many missense variants contribute to the signal as well (Fig. 4d).
Finally, we investigated what proportion of the gene-based signals could be traced back to one causal variant as opposed to requiring the grouped effects of multiple rare variants to achieve significance. First, we found that only 16% of the significantly associated genes had a single variant within the gene whose p value was statistically significant after multiple test correction. Of these, we found that only 7% of associations had a single variant with a better p value than the gene as a whole. Second, we re-analyzed the significant associations after including the lead variant for each gene as a covariate (except for four associations where all qualifying variants in the gene had two or fewer carriers; Supplementary Data 2). After factoring out the signal from the most significant variant in each gene, we found that 41% of associations had their p values rise sufficiently to fail statistical significance: yet, 85% of the associations still generated a p value below 5 × 10−8 with the lead variant accounted for, and only 2% clearly had their entire signal driven by the lead variant (p > 0.05 after removing lead variant). Together, our results indicate that while some significant associations had single variants that made major contributions to their effects, few were completely explained by individual variants.
17 Common iPhone 8 Problems & How to Fix Them
If you’re dealing with an iPhone 8 or iPhone 8 Plus problem you should try a fix from the list below before taking your phone into a store.
Apple’s iPhone 8 and iPhone 8 Plus are solid devices, but they’re far from perfect. Many iPhone 8 users are running into issues with the two devices and we expect complaints to grow as we push into 2020.
Many of the current iPhone 8 problems are extremely common. We’re seeing complaints about sound issues, wonky battery life, problems with Bluetooth, 3D Touch issues, random reboots, and more.
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If you start noticing issues with your new phone you might be tempted to get in touch with Apple or schedule an appointment at your local store. Before you do that you should try fixing the problem yourself. Most iPhone issues can be solved within minutes from the comfort of your home or office.
Our guide here takes a look at the most common iPhone 8 problems and shows you how to fix them. There’s no guarantee these will work for you but they’re worth a shot if you start noticing performance issues or bugs on your iPhone 8 or iPhone 8 Plus.
How to Fix iPhone 8 iCloud Restore Problems
If your iPhone 8 or iPhone 8 Plus gets stuck updating iCloud Settings you’ll want to hold down the Power button and Volume Down and wait for the device to reboot itself. Once it reboots, try the process again.
If you encounter iCloud Restore problems, create a local backup on your computer and then restore the backup to your iPhone 8. This workaround worked for us in the past and it might work for you.
If you’re unable to get your old iPhone’s data backed up, check out our list iCloud backup problems and fixes. Apple’s also released a guide that takes you through some of the most common iCloud backup issues. You might check there as well.
How to Fix iPhone 8 Battery Life Problems
iPhone battery life issues are extremely common and there’s a chance you’ll start seeing abnormal battery drain on your iPhone 8 or iPhone 8 Plus. Fortunately, it’s probably not the hardware that’s causing the problem.
If you start noticing weird battery drain on your iPhone 8 you’ll want to dig into your apps and your software. To assist you, we’ve put together a guide to improving iPhone 8 battery life. This is a great place to start if you don’t know where to turn.
When a new iPhone 8 update is available you might think about installing it right away. While iOS updates typically don’t mention battery life improvements in the change log there’s always a chance a new update will work wonders.
How to Fix Swelling iPhone 8 Battery Problem
It appears that some iPhone 8 batteries are starting to swell up. The issue is impacting users around the world including here in the United States.
Unfortunately, there’s no way to fix this issue on your own right now. Apple is investigating, but you’ll want to get in contact with Apple Support if your iPhone 8 battery starts to swell.
How to Fix iPhone 8 Performance Problems
We’ve encountered a bit of lag on the iPhone 8 models in our possession and others are seeing similar issues.
If you encounter lag, occasional freezes, and general sluggishness, you’ll need to take action. To help, we’ve put together a guide that will take you through some strategies to use when your iPhone runs slower than usual.
Sometimes it can take a few days for new software to settle in so if you start noticing issues after installing a software update give it a few days before taking drastic actions.
How to Fix iPhone 8 Wi-Fi Problems
Some iPhone 8 users are reporting issues with Wi-Fi connectivity. Wi-Fi problems are extremely common and they can popup at any time. Unfortunately, they can be tricky to fix.
First you’ll want to make sure it’s not an issue with your router or ISP (Internet Service Provider). Restart your router (unplug for a minute and plug back in) and see if that jumpstarts the network and speeds. If you’re positive it’s not an issue with your router, router’s firmware, or ISP, here are a few fixes to try.
If you’re experiencing slower than normal download/upload speeds, you can try resetting your device’s network settings.
This will cause your device to forget your Wi-Fi passwords so make sure you have those handy before you do this.
If that doesn’t help you’ll want to forget the Wi-Fi network giving your iPhone 8 issues:
This will also cause your device to forget the Wi-Fi password so make sure you have that on hand.
You should also restart your iPhone 8 or iPhone 8 Plus. This only takes a few seconds but it’s been known to dislodge various Wi-Fi issues.
If those fixes don’t work, Apple’s released its own guide to iPhone Wi-Fi problems. Take a look there before scheduling an appointment.
How to Fix iPhone 8 Frozen Screen
If your iPhone 8’s screen suddenly locks up and you’re unable to unfreeze it pressing the home button, you’ll need to perform a hard reset.
To do that, press Volume Up and release, press Volume Down and release, and then hold the power button for about 5-10 seconds.
How to Fix iPhone 8 Bluetooth Problems
Bluetooth issues are affecting many iPhone 8 and iPhone 8 Plus users. Some users are reporting issues connecting their Bluetooth headphones which is problematic given that neither device features a 3.5mm headphone jack.
Like Wi-Fi issues, Bluetooth problems can be difficult to fix (particularly if you’re dealing with issues in your car) but here are a few remedies to try.
The first thing you’ll want to do is head into your Settings then go to Bluetooth, select the Bluetooth connection having issues using the “i” in the circle, and then tap Forget this Device. Try reconnecting. This has worked for us, and many others, in the past.
If that fails, go to your iPhone 8’s Settings, tap General, tap Reset, and tap Reset Network Settings. Try reconnecting to the device. Make sure you have your Wi-Fi passwords handy because this will cause the device to forget them.
You might also try resetting your iPhone 8’s settings to its factory defaults. Go to Settings, tap General, tap Reset, and tap Reset All Settings. This might take a few minutes to finish up and it will also cause the device to forget Wi-Fi passwords.
If you’re dealing with Bluetooth issues in the car and those fixes don’t help, you’ll need to consult your car’s manual. If you’re unable to reset the connection you might want to make an appointment with customer service at your local dealership to see if they can help.
How to Fix iPhone 8 Sound Problems
If your iPhone 8’s speakers or microphone start acting up, here are some things to try.
If you’re noticing a crackling sound, make sure you’re running the latest version of iOS.
Next, check the Ring/Silent switch on the side of your device to make sure it’s set in the right position. You might’ve accidentally nudged it while holding the phone.
If it’s set correctly, try restarting your iPhone 8. Hold down the power button and turn the phone off. Power it back on and check the sound.You can also try performing a hard reset.
If that doesn’t help, try turning Bluetooth off and on. Check the sound. If it’s still missing, try removing any dust or debris that could be blocking the speaker grille or the Lightning Dock.
If your microphone suddenly stops working or starts randomly cutting out, restart your phone. You can also try restoring your phone from a backup to see if that works. If it still doesn’t work, get in touch with Apple because you might be dealing with a hardware issue.
How to Fix Poor iPhone 8 Call Quality
If you start noticing a sudden drop in call quality the first thing you’ll want to do is restart your phone. Politely hang up the phone and reboot the iPhone 8 or iPhone 8 Plus.
If this doesn’t work, check the iPhone’s receiver to make sure it isn’t blocked. The receiver is that little slit located above the iPhone 8’s screen. There could be debris buildup or it could be that your screen protector is blocking it.
You can also try removing your case (if you’re using one), disabling Bluetooth (there could be interference due to another device in the area), or switching LTE from Voice & Data to just Data. To do that head into Settings, go to Cellular, tap Cellular Data Options, tap Enable LTE, and then tap Data Only.
You’ll also want to make sure you’re running the latest version of iOS.
What To Do If Your iPhone 8 Can’t Connect to the App Store
If your iPhone 8 suddenly can’t connect to the App Store, make sure Apple’s service isn’t down. If it’s up, here are a few quick fixes to try:
Our other workaround requires a bit of work. First, you’ll want to sync the date and time on your iPhone by going to General and then Date & Time. Toggle Set Automatically to off then scroll down to set the data and time manually.
Go to the App Store, leave it open for a few seconds, and then go back to Date & Time and toggle Set Automatically to on. Close the App Store in your multitasking tray and then open it up again and see if you can establish a connection.
How to Fix iPhone 8 Random Shut Off
If your iPhone 8 or iPhone 8 Plus starts randomly restarting itself there’s no need to panic. At least not yet.
If your device starts restarting itself more than once a day hold down the Volume Down button and the Power button at the same time and wait for the phone to reboot itself. This has (temporarily) cleared up the issue for us and others in the past.
If your phone is randomly rebooting itself more than a few times a day you might want to get in touch with Apple customer service.
How to Fix iPhone 8 3D Touch Problems
Like the iPhone 6s and iPhone 7, the iPhone 8 comes with 3D Touch. 3D Touch lets you make hard presses on the screen to open up shortcuts and features.
3D Touch is giving some iPhone 8 users problems. It’s popping up too fast for some users and some users are having trouble getting the shortcuts to popup.
If you’re having issues with 3D Touch, you’ll want to adjust the feature’s sensitivity to better suit your needs. To do that, head into Settings, tap General, tap Accessibility, and scroll down to 3D Touch and tap.
The default should be set to medium but you can switch it to firm or light. Go ahead and test it at the bottom of the screen.
If that doesn’t fix your problem try resetting your settings. Head to Settings, tap General, tap Reset, and then tap Reset All Settings. Your device will forget known Wi-Fi passwords but you won’t lose any data.
You can also try restarting your phone.
How to Fix iPhone 8 Cellular Data Problems
If your iPhone 8 suddenly displays the “No Service” symbol and you can’t connect your cellular provider’s network, we’ve got a few things for you to try.
First, check your service provider for outages. Outages are common so poke around on social media sites for updates. You’ll also want to check sites like Down Detector.
If you’re confident that it’s not a data outage, try restarting your device. Power it down and then power it back on to see if that helps.
If that doesn’t work, flip on Airplane Mode for 30 seconds before turning it off. Airplane Mode kills all connections on your device and it could fix your problem.
Next, toggle Cellular Data and/or LTE off and on to see if that helps. To shut LTE down temporarily, go into Settings, then Cellular, then Cellular Data Options, and then toggle Enable LTE to Off. Turn it back on when and if you need it.
To shut off Cellular Data completely without turning off any other services go to Settings, then Cellular, then toggle Cellular Data to Off. Toggle it back on when you need to.
How to Fix iPhone 8 Overheating Problems
Your iPhone 8 or iPhone 8 Plus might feel hot if you’re playing a game or running something intensive. That heat should go away after awhile. If it doesn’t, here are a few things to try.
Restart your phone. If that doesn’t calm things down, check for apps that might be drawing an abnormal amount of power from your phone. If you notice something out of the ordinary you might want to re/uninstall the app and/or wait for a new bug fix update.
You can also try turning off location services as these can put heavy strain on your phone. To do that, go to Settings, then Privacy, then Location Services, and toggle it off at the top.
If that still doesn’t help, try restoring your iPhone 8/iPhone 8 Plus. If restoring fails, you’ll want to get in touch with Apple customer service about a potential replacement.
How to Fix iPhone 8 Apps Freezing & Quitting
If the apps on your iPhone 8 or iPhone 8 are continually freezing or quitting, here are a few fixes that might squash the issue.
First, restart your phone.
If that doesn’t help you’ll want to check the App Store for an update. Developers have been trotting out support updates and the latest version could stabilize the app. Make sure you read reviews from iPhone 8 users before you install. You can also delete the app and download it again to see if that helps.
If that doesn’t fix the issue, get in contact with the developer and see if its aware of the problem. If it is, it might have a workaround or an ETA on a bug fix update.
How to Fix an Unresponsive iPhone 8 Display
If your iPhone 8’s touchscreen becomes unresponsive, the first thing to do is hard reset the device. Hold down the phone’s Power Button and the Volume Down button at the same time and wait for the phone to reboot itself.
If it’s happening in a specific app, close the app and reopen it. Double tap on the home button, close the app in the multitasking tray and open it again.
You’ll also want to make sure your screen is clean and dry.
If your touchscreen suddenly stops working and you repaired your iPhone 8 or iPhone 8 Plus at a third-party store, you’ll want to install the latest version of iOS.
How to Fix iPhone 8 Wireless Charging Issues
If you’re unable to charge your iPhone 8 or iPhone 8 Plus or if your device is charging slowly, here are a few things to try.
Make sure you put the iPhone 8 on the center of the charger, or it may not charge.
If wireless charging isn’t working and you use your iPhone 8 case to store credit cards or security passes, make sure you remove those before charging. You also might try taking your case off.
If you’re using a third party accessory to charge your iPhone 8 or iPhone 8 Plus, make sure the device is Apple certified. You can do that via Apple’s website.
How to Fix iPhone 8 Problems If Nothing Else Works
If you can’t find a fix for your iPhone 8 or iPhone 8 Plus problem on our list here are a few recommendations.
First, install the latest iOS update. Apple’s released a new iOS 13 update that tackles issues plaguing the iPhone 8 and iPhone 8 Plus.
If that doesn’t work, head to Apple’s discussion forums and ask for help. Be sure to do it in the right place. You can also ping Apple Support on Twitter or make contact with support on the company’s website.
If Apple’s online customer service is unable to help, you can try downgrading to an older version of iOS when the option is available.
If you can’t or don’t want to downgrade, you can schedule an appointment to see a Genius provided you have an Apple Store near where you live.
If you don’t want to take it into a store, you can start fresh on your own.
Factory resetting your device will wipe everything stored on your iPhone 8 and return it to the way it was when you first opened the box so make sure you backup all of your important data before you make the move.
Once you’ve backed up all of your files, go to Settings, then General, then Reset, and then Erase All Content and Settings. Again, this should only be used as a last resort.
4 Reasons Not to Install iOS 13.3.1 & 11 Reasons You Should
Install iOS 13.3.1 for Better Security 
If security is important to you, think about installing the iOS 13.3.1 update right away.
The iOS 13.3.1 update includes 21 new security patches that will help protect your device from harm. The company's outlined those patches in detail if you want to dig in.
If you skipped iOS 13.3, you get its patches with iOS 13.3.1. iOS 13.3 brought 12 new security patches to the iPhone and you can read about each one over on Apple's security page.
The iOS 13.3 update also added support for NFC, USB, and Lightning FIDO2-compliant security keys in the Safari browser.
If you missed iOS 13.2, it had 16 new security patches on board. You can read about all of them on Apple's website right here.
iOS 13.1.1 brought a security patch for a third-party keyboard issue to your iPhone. If you're interested in the particulars, you can read about them over on Apple's website.
If you passed on installing iOS 13.1, you get an additional patch with your iOS 13.3.1 update. You can learn more right here.
If you're moving up from iOS 12, you'll get iOS 13.0's nine security patches with your upgrade to iOS 13.3.1. Read about those here.
If you skipped iOS 12.4.1 or any older versions of iOS 12, you'll get their security patches with your iOS 13.3.1 update.
iOS 12.4.1 only had one patch on board, but Apple's iOS 12.4 brought 19 security patches to the iPhone. If you're interested in the specifics, you can read about them on right here.
In addition to those patches, iOS 13 itself comes with some security and privacy upgrades including improved anti-tracking features in Safari and the ability to get rid of location metadata in your photos.
You also now have the ability to block apps from using Bluetooth and the ability to allow apps to access your location just once.
iOS 13 will also send you reminders about applications that track your data.
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