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. 2022 May 6;5(2):380–400. doi: 10.20517/cdr.2021.125

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© The Author(s) 2022.

© The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, 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.

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Binding of BH3 mimetic, Venetoclax to BCL-2 anti-apoptotic protein releases bound BH3-only protein, subsequently allowing interaction between BH3-only protein and BAK/BAX. Upregulation of MCL-1, BCL-xL, and BCL2-A1 confers Venetoclax resistance by sequestration of BH3 only proteins, preventing them from interacting with BAK/BAX and avoidance of apoptosis^[35-40].