Accordingly, various studies showed that targeting MCL-1, either through genetic- or BH3 peptide-based approaches, makes resistant cells significantly more sensitive to BCL-XL/BCL-2 inhibition, and abrogates growth of MCL-1-dependent cancers (e.g. AML and MYC-driven lymphoma) [74,93–96]. Here, MCL1 is linked to acute myeloid leukemia.