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. 2023 Mar 9;14:1290. doi: 10.1038/s41467-023-37013-x

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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. 9 — HP1γ-MDC1 complex recognizes the DSB sites and exerts the function of DNA repair, as well as how the nuclear condensation of HP1γ is regulated by deacetylation and facilitated by MDC1; HP1γ remodels histone methylation to facilitate accessibility of genes governing sensitivity to PIs; therefore, targeting HP1γ may be efficacious for overcoming drug resistance in MM patients.