We used our established genetic model in TrC1 prostate cancer cells expressing either AKT1-WT or the clinically relevant activation associated AKT1-E17K mutant and pharmacologic approaches to explore how cancer cell-specific aberrant AKT activation and the activity of AKT-regulated metabolic pathways impact metabolic state and antioxidant defense at the basal state as well as changes in cellular levels of GSH, NADPH, and ROS, short-term and long-term survival upon irradiation. The gene discussed is AKT1; the disease is prostate carcinoma.