Whereas p53 is mostly unmutated in AML, it is often inactive due to suppression by antagonistic factors, mostly Mdm2 and MdmX frequently amplified in AML.(16, 33) Attempts to inactivate Mdm2 inhibition as therapeutic means in AML are ongoing for many years with moderate success.(31, 32) Increasing p53 activity and suppressing expression of anti-apoptotic proteins represents a potential therapeutic strategy for improving outcomes in R/R myeloid malignancies and more broadly, other malignancies. Here, TP53 is linked to acute myeloid leukemia.