Nevertheless, we have previously shown the utility of disrupting proapoptotic Bcl-2 protein interactions in CLL, WM and multiple myeloma and that this functional interference results in malignant cell death or resensitization (or heightened sensitivity) of tumor cells towards other therapeutics.15, 25, 35, 40, 45, 46, 47, 48, 49, 50, 51 Indeed, this observation also held true for CXCR4WHIM-like-negative ibrutinib-resistant WM cells, where the Bcl-2-specific BH3 mimetic, venetoclax, decreased ibrutinib-resistant WM cell viability and induced apoptosis as a single agent. Here, BCL2 is linked to AL amyloidosis.