Despite remarkable advances in the treatment of NPM1-mutated AML, due to optimization of conventional induction chemotherapy and risk-stratified consolidation with cytarabine and HSCT in first remission in younger patients, and development of novel therapeutic approaches including BCL-2 inhibitor venetoclax and hypomethylating agent association, immune checkpoint inhibitors and AML-targeted monoclonal antibodies in older unfit patients, about 50% of patients still die of progressive disease [12,21,22]. Here, BCL2 is linked to acute myeloid leukemia.