IKKα further contributes to the activation of AKT through physical association with mTORC2, leading specifically to the AKT-dependent phosphorylation and inhibition of Forkhead box O3a (FOXO3a) and GSK3β, but not other AKT targets, such as Tuberous sclerosis complex subunit 2 (TSC2) and proline-rich AKT substrate of 40 kDa (PRAS40) in several cancer cells [143]. The gene discussed is AKT1; the disease is cancer.