Indirect targeting of MCL-1 through CDK9 inhibition potently sensitizes non-Hodgkin Lymphoma and AML cells to the BCL-2 inhibitor venetoclax without significant toxicity to mice suggesting that this strategy to co-target multiple pro-survival BCL-2 proteins could be tolerable if applied to breast cancer in the clinic [61,63]. This evidence concerns the gene MCL1 and acute myeloid leukemia.