AKT1 and neoplasm: Studies in experimental models of prostate cancer provided evidence that GNPNAT1 inactivation increased the aggressiveness and proliferation capacity of prostate cancer cells, through either activation of PI3K-AKT pathway in cells expressing FL-AR or by specific protein 1 (SP1)-regulated expression of carbohydrate response element-binding (ChREBP) in tumor cells expressing AR-V7 [464].