To identify the precise downstream effectors activated by AKT to regulate AML-M5 cell survival, we examined the expression of GSK3β, FOXO1A, BCL-2, BAX, and the cyclin-dependent kinase inhibitors (CDKIs) P27 and P21, which regulate cell survival and physiology (38–41). The gene discussed is FOXO1; the disease is acute myeloid leukemia.