In this case, a more in-depth molecular analysis of the mechanisms underlying the cellular response showed that sunitinib decreased the MCL-1 expression more than the BCL-2 (Figure 3C; *p < 0.05, **p < 0.01, ***p < 0.001), supporting that KMT2A-AML cells were susceptible to venetoclax treatment due to the effects induced in MCL-1. Here, MCL1 is linked to acute myeloid leukemia.