The overexpression of TGF-β may stimulate the transition of epithelial–mesenchymal (EMT) and renal sclerosis, resulting in renal dysfunction [17,18] and indicating that the anti-TGF-β1 antibody exerts suppressive effects on fibrotic gene activation when administered after the onset of proteinuria in two distinct mouse models of glomerulonephritis. Here, TGFB1 is linked to glomerulonephritis.