Moreover, we demonstrate that the overexpression of the Akt1-TASA mutant that is deficient in phosphorylation of Akt’s two major activation-associated phosphorylation sites, T308 and S473, decelerated the repair of radiation-induced DSB and increased radiosensitivity of TrC1 prostate cancer cells when compared to Akt1-WT overexpressing TrC1. The gene discussed is AKT1; the disease is prostate carcinoma.