Moreover, we established murine TrC1 prostate cancer cells stably overexpressing phosphorylation-deficient Akt1 mutants including Akt1-T308A (Akt1-TA), -S473A (Akt1-SA) and -T308A/S473A (Akt1-TASA) and determined the effects of this overexpression on DNA DSB repair as well as on its survival upon exposure to ionizing radiation (IR). This evidence concerns the gene AKT1 and prostate cancer.