With time, intensive fibrosis reactions induced by hyperglycemia in glomerular mesangium, including increased levels of inflammatory and profibrotic mediators such as TGF-β1, as well as increased accumulation of extracellular matrix proteins such as fibronectin and collagens, ultimately lead to diabetes-induced renal failure3, 4, 5. This evidence concerns the gene TGFB1 and diabetes mellitus.