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. 2020 Jul 29;11:3696. doi: 10.1038/s41467-020-14743-w

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© The Author(s) 2020

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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Fig. 5 — a Mutation status in extended genes can explain expression differences for a larger number of genes than other annotations, such as annotations of coding sequences (CDS). b A 130-kbp deletion in the breast cancer cell line T47D potentially links a distal enhancer to the promoter of ERBB4, leading to its activation. This change does not affect coding sequences, highlighting the value of an extended gene annotation. c Cancer-associated GWAS SNVs display greater enrichment with the inclusion of proximal and distal annotations in extended gene definitions. d Somatic structural variant breakpoints in K562 tend to be associated with the activating histone mark H4K20me1, but not in GM12878.