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. 2022 Dec 20;13(12):1059. doi: 10.1038/s41419-022-05505-1

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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. 1 — Brd4 can inhibit apoptosis through both intrinsic (mitochondrial) and extrinsic (death receptor-mediated) mechanisms by regulating the expression of many key components of these pathways. Brd4 directly or indirectly either upregulates the expression of genes coding anti-apoptotic proteins (BCL-2, BCL-xL, MCL-1, LIVIN, cFLIP, XIAP, Survivin and cIAP2) or downregulates the expression of genes coding pro-apoptotic proteins (NOXA, PUMA, BIM and CHOP).