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. 2022 Aug 11;54(9):1406–1416. doi: 10.1038/s41588-022-01147-3

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Extended Data Fig. 8 — More mutations in hiPSCs were discovered in fibroblasts (shared mutations) through high-coverage Whole Exome Sequencing (hcWES) than through WES, resulting in the percentage of shared mutations increased in hcWES data. Interestingly, the mutational profile of these increased shared mutations is very similar to the UV signature, indicating that increasing sequencing depth enables more UV-caused somatic mutations that were found in hiPSCs to also be detected in the corresponding fibroblasts.