In particular, aberrant overexpression of BCL-2, together with other anti-apoptotic proteins as BCL-XL and MCL-1, has been detected in AML cells [24,25,26], where suppressed mitochondrial-modulated programmed cell death, supports cell survival [27], mediates chemoresistance and confers survival benefits [28]. This evidence concerns the gene MCL1 and acute myeloid leukemia.