AKT1 and neoplasm: As AKT is a potent activator of glucose uptake and glycolysis, tumors dependent on PI3K/Akt signaling could shunt the glucose-6-phosphate (G6P) generated during glycolysis to the PPP activated by Nrf2, thus maintaining a stable pool of NADPH, which could be used for anabolic processes to sustain tumor growth and proliferation, or ROS detoxification (77, 78) (Figure 2).