Activation of PI3K/mTOR pathway and overexpression of Mdm2 are frequent molecular features in Acute Myeloid Leukemia (AML): according to the interactions between PI3K/mTOR and Mdm2/p53 pathways, Kojima and colleagues demonstrated that treatment with PI-103 (a dual PI3K/mTOR inhibitor) enhances p53 downstream signaling in p53 wild-type AML contexts [82]. This evidence concerns the gene TP53 and acute myeloid leukemia.