Another study from the same group [57] established that phosphorylation of AKT on Thr308 and Ser473 increases following treatment of ALL cells with AICAR and demonstrated that AKT phosphorylation on Thr 308 is mediated by AMPK-induced IGF-1R activation and phosphorylation of IRS-1. This evidence concerns the gene AKT1 and acute lymphoblastic leukemia.