The antiapoptotic protein MCL1 is overexpressed in AML cell lines resistant to venetoclax.(12) Similarly, the sensitivity of AML patients samples to venetoclax inversely correlates with the presence of a TP53 mutation or low expression of P53.(13) In AML, P53 inactivation commonly results from overexpression of its negative regulators, MDMX and MDM2.(14–16). The gene discussed is TP53; the disease is acute myeloid leukemia.