The increase in lactate secretion from cancer cells, on the other hand, might be attributable to two distinct mechanisms: 1) high glucose directly activates AR/PP leading to the over-production of fructose and lactate; 2) overexpressed AR interacts with AKT1 to augment AKT/mTOR, HIF1a and PKM2 signaling, eventually leading to increased flux through the aerobic glycolysis to enhance lactate formation. The gene discussed is MTOR; the disease is cancer.