In addition, PP2A dephosphorylates Akt at both Thr308 and Ser473 sites, resulting in consequent apoptotic pathway activation13, and PP2A inhibition has been suggested as potential cancer treatment and knockdown of PP2A in several in vitro cancer cell models resulted in elevated γH2AX and increased radiosensitivity14–17. This evidence concerns the gene AKT1 and cancer.