TGF‐β is considered as one of the most relevant pro‐fibrotic factors accounting for glomerulosclerosis and interstitial fibrosis in DKD as well as other chronic nephropathies.52, 53 The administration of anti‐ TGF‐β antibodies, antisense TGF‐β1 oligodeoxynucleotides or knocking off the downstream Smad3 gene prevent and/or reverse the hypertrophic and pro‐fibrotic effects of hyperglycaemia in DKD.54 Here, SMAD3 is linked to glomerulosclerosis.