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. 2021 Jun 8;13:124. doi: 10.1186/s13148-021-01110-9

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — DNA methylation differences between TAD and healthy control samples. a DMR percentages in different genomic components (promoters were defined as 1–2,500 bp upstream of transcription start site, alternative promoters were not included.). b Hypermethylated and hypomethylated DMR percentages in different genomic components. c Supervised clustering with the top 300 DMRs (detail information was showed in Additional file 2: Table S3). d Gene ontology (GO) enrichment analysis with a focus on biological processes for the hypomethylated DMRs