Therapeutic agents that target the TGFβ/smad signalling pathway to reduce scarring have been successful in pre‐clinical studies.7 Inhibitors of the TGFβ receptor ALK5 decreased TGFβ activity, rescued cardiac dysfunction and ameliorated the remodelling that occurs post‐MI.47 In a bleomycin‐lung fibrosis model, the fibrotic process was attenuated in mice lacking smad3.48, 49 We examined the attenuated expressions of collagen I, collagen III, smad2, p‐smad2, smad3, p‐smad3 and smad4 in the Ang II + rTGFβ3 groups. This evidence concerns the gene SMAD4 and pulmonary fibrosis.