TP53 and acute myeloid leukemia: The biological mechanisms of this susceptibility may be as follows: the G allele of MDM2 -309T>G polymorphism could significantly increase the affinity of MDM2 to transcriptional activator SPl, resulting in increased mRNA transcription and protein expression of MDM2. Thus, MDM2 directly inhibits the p53 tumor suppressor pathway and increasing risk of AML in people with mutant allele (G).