Studies have now demonstrated that TGF‐ β1 signalling through type I TGF‐β receptors leads to phosphorylation and nuclear translocation of Smad2 and Smad 3 that promotes renal fibrosis, while the overexpression of Smad7 prevents TGF‐ β1‐mediated renal fibrosis.11, 12. The gene discussed is SMAD2; the disease is renal fibrosis.