In addition, AML also exhibits resistance mechanisms mediated by mutations in the tumor suppressor gene TP53. Full TP53 function is critical for BH3-mimetic drugs efficacy, and if TP53-mutant clones emerge under the therapeutic pressure of sublethal doses of BCL-2 or MCL-1 inhibitors, drug resistance will occur (89). This evidence concerns the gene TP53 and acute myeloid leukemia.