Renal mTOR activation in poorly controlled diabetes may result from a combination of AKT inhibition of TSC2, hyperglycemia-induced AMP kinase inhibition and increased glucose uptake through glucose transporter 1 (GLUT1), in which the resulting increased glycolysis and activation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) can lead directly to Rheb activation of mTOR by reducing Rheb binding to GAPDH [37,38]. The gene discussed is RHEB; the disease is Hyperglycemia.