We show that the mechanism of Akt activation in ALL cells is mediated in part by AMPK-induced phosphorylation of IRS-1 at Ser794, the immediate downstream effectors of the IGF-1R signaling cascade, and also in part by AMPK-induced inhibition of mTOR and its downstream feedback loop inhibition of IRS-1 (Ser312). The gene discussed is AKT1; the disease is acute lymphoblastic leukemia.