Given that MCL-1 overexpression confers resistance to venetoclax and that there is favorable synergy in combinatorial targeting of MCL-1 and BCL-2 in multiple myeloma and acute myeloid leukemia [23–26], we hypothesized that AZD5991 may restore venetoclax efficacy and induce synergistic lethality in venetoclax-resistant MCL cells. This evidence concerns the gene BCL2 and AL amyloidosis.