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. 2020 Nov 30;124(4):770–776. doi: 10.1038/s41416-020-01191-y

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© The Author(s) 2020

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. 4 — PI treatment induced MM cells to enter epigenetic alteration-mediated reversible tolerance. Exposure to further chemotherapy and selection can ‘lock in’ an epigenetic state, resulting in proliferation of a hardwired drug-resistant population. However, combination with HDAC inhibitors (HDACis) and high-dosage intermittent therapy can reverse epigenetic tolerance and prevent the emergence of PI-tolerant cells. TME tumour microenvironment, ECM extracellular matrix.