We have dissected this to some degree via treatment with the mTOR inhibitor rapamycin (mTORC2 is an essential AKT activator for FOXO regulation 37) and the PI3K inhibitor LY294002 to determine whether these drugs were able to inhibit phosphorylation of FOXO1, 3a, and 4 and thus restore FOXO activity in CD34+ CML cells. The gene discussed is AKT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.