Considering the known adverse effect of TP53 mutations in AML in general, and specifically as our data indicate in R/R AML treated with HiDAC/MITO salvage therapy, it is hoped and anticipated that specific targeting of wild-type and mutated TP53 via MDM2, the main negative regulator of TP53, may improve patient outcomes. The gene discussed is MDM2; the disease is acute myeloid leukemia.