Potentially, this effect could be enhanced with dual inhibition of both MDM2 and MDMX, for example using a stapled α-helical peptide called ALRN-6924, which has been previously shown to be very effective in xenograft models with p53 wildtype AML.118 Another strategy to increase the apoptotic priming of EVI1high leukemias could be treatment with BH3 mimetics such as venetoclax, that target anti-apoptotic BCL2 family members. This evidence concerns the gene TP53 and acute myeloid leukemia.