We previously demonstrated that Smad3 is a key Smad protein that mediates fibrosis in multiple organs and tissues.3, 28 Inhibition of Smad3 using specific inhibitors reduces fibrosis.39, 40, 41, 42 In this study, we found that petA is a potential inhibitor of TGF‐β/Smad3 activation, which suggests that petA may relieve renal fibrosis as well as cirrhosis, cardiac fibrosis and lung fibrosis. This evidence concerns the gene SMAD3 and pulmonary fibrosis.