While it has been demonstrated [12–16] that co-treatment with venetoclax and a selective inhibitor of another redundant pro-survival protein (such as Mcl-1) can overcome resistance to Bcl-2 inhibition in AML, both Mcl-1 [17–20] and Bcl-XL [21–23] are vital for the survival of normal blood cells. Here, BCL2 is linked to acute myeloid leukemia.