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). Here, AKT1 is linked to prostate carcinoma.