ERK1/2, the effector of the RAS–RAF–MEK pathway, has been shown to stabilize c-MYC protein by phosphorylation at Ser62.16 Activation of AKT results in GSK3β phosphorylation, thereby inhibiting the normal function of GSK3β in destabilizing c-MYC via phosphorylation at Thr58.16 Hence, an increase in c-MYC protein stability can be expected when ERK1/2 and AKT are activated, which is common through gain-of-function mutations in RAS17 or loss-of-function mutations or deletion of PTEN18 in prostate cancer. This evidence concerns the gene AKT1 and prostate carcinoma.