HG and hemodynamic changes in this early stage may be responsible for the activation of the Notch signaling pathway.[18] HG stimulates the glomerular mesangial cells to produce large amounts of transforming growth factor-β1 (TGF-β1) and reduce the degradation of EMC at the same time, causing glomerular sclerosis.[19,20] Zhang et al[21] reported that miR-34a regulated mesangial proliferation and glomerular hypertrophy by directly inhibiting GAS1 in early DN. The gene discussed is TGFB1; the disease is glomerulosclerosis.