Constitutive activation of PI3K/AKT, at least in part, results from autocrine IGF-I release and activation of IGF-IR, which was shown in 70% of AML samples [18, 57]Several in vitro studies using different IGF-IR inhibitors illustrated the therapeutic potential of targeting IGF-IR in AML. This evidence concerns the gene AKT1 and acute myeloid leukemia.