Glomerular mesangial hypertrophy and ECM accumulation induced by HG, TGF-β, oxidant stress and related stimuli are relatively early events in the pathogegesis of DN, which can trigger pathological effects in other renal cells (podocytes, tubular, endothelial cells) and ultimately lead to end stage of renal disease. This evidence concerns the gene TGFB1 and kidney disorder.