mTOR pathway signaling abnormalities seem to be present in all the key steps of DN progression, including (i) podocyte damage and loss, an early event in DN that further causes glomerulosclerosis; (ii) overactivation of mesangial cells that promotes increased ECM synthesis and decreased degradation of damaged podocytes; (iii) glomerular endothelial cells and mesangial cell crosstalk that precedes glomerulosclerosis; and (iv) fibrosis and epithelial-to-mesenchymal transition in tubulointerstitial cells [11]. The gene discussed is MTOR; the disease is liver dysplastic nodule.