As a result of hyperglycemic stimulation of PI3K and inhibition of PTEN, the Akt/mTOR pathway is activated, leading to the development of DN through abnormal podocyte autophagy, renal fibrosis, enlargement of the mesangial matrix and thickening of the basement membrane (Estacio and Schrier, 2001). The gene discussed is AKT1; the disease is liver dysplastic nodule.