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. 2022 Oct 2;13:5789. doi: 10.1038/s41467-022-33461-z

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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. 7 — a, b Clonal plasma cells isolated from Kappa- and Lambda-predominant AL amyloidosis were isolated and BH3 profiled to measure their a overall level of apoptotic priming via sensitivity to the BIM BH3, BID BH3, and PUMA BH3 peptides and their b dependencies on the pro-survival BCL-2 family proteins BCL-2, BCL-X_L, and MCL-1. c–e BH3 profiling indicating (c) overall apoptotic priming and d BCL-2 family dependencies in clonal plasma cells from AL amyloidosis patients with t(11;14), and e ex vivo sensitivity to BH3 mimetics. f, g BH3 profiling CD138 + cells from a healthy bone marrow donor showing (f) overall priming and g dependencies on pro-survival proteins compared to clonal AL CD138 + cells. h Dynamic BH3 profiling of normal plasma cells treated with bortezomib for 12 h. i Ex vivo sensitivity of normal plasma cells to the combination treatment of bortezomib with indicated BH3 mimetics. P-values were calculated using two-way ANOVA with Holm–Sidak’s adjustment for e.