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. 2022 Sep 28;41(44):4841–4854. doi: 10.1038/s41388-022-02471-y

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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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Fig. 6 — A–F THP1 AML cells were infected with lentiviral vectors targeting HMG20B for KD, or a non-targeting control (NTC) and selected for puromycin resistance. A Heatmap shows differentially expressed genes 72 h after initiation of KD. B Summary table and representative GSEA plots. C, D GSEA plots. E, F HMG20B binding peaks were grouped into ten cohorts according to peak strength and mapped to nearby genes to generate gene sets for use in GSEA. Graphs (right panels) show false discovery rates by cohort for genes bound by HMG20B at E promoters and F putative enhancers. GSEA plots are shown for the top cohorts (left panels).