Because VEN is a selective inhibitor of BCL2 protein expressed in AML, other anti-apoptotic BCL2 proteins, such as BCL-xL (74), MCL1 (66, 67, 75), BCL2A1 (76, 77) and BFL1 serve as mediators for primary or acquired secondary resistance to VEN by leukemic cells, via alterations of the apoptotic pathways (5–7, 69). This evidence concerns the gene BCL2L1 and acute myeloid leukemia.