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. 2023 Jun 12;15:101. doi: 10.1186/s13148-023-01491-z

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© The Author(s) 2023

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 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. 7 — The default transcriptional state of pancreatic ductal progenitors is hypothesized by high EZH2 activity suppressing the expression of endocrine genes such as INS, NGN3 and PDX1. Inhibition of EZH2 restores the progenitor capacity in ductal cells, reducing the H3K27me3 mark and allowing for transcription of genes that influence differentiation into β-like cells