Although TP53 mutations are more common in some AML subgroups, p53 inactivation is more likely to be caused by the overexpression of its endogenous inhibitors, like mouse double minute 4 homolog (MDMX) or mouse double minute 2 homolog (MDM2), which frequently occur in TP53 wild-type AML [120]. Here, MDM2 is linked to acute myeloid leukemia.