It is ubiquitously distributed and has been recognized as one of most powerful pro‐fibrogenic mediators.11 Upon activation, TGF‐β may bind to type I and type II serine/threonine kinase receptors and then activate receptor‐regulated Smads including Smad3.12 Previous studies have shown that TGF‐β/Smad signalling pathway inactivation may relieve the hepatic fibrosis.13, 14 The present study manifested that the higher expression of TGF‐β1 and ratio of p‐Smad3/Samd3 were observed in CCl4‐treated rats. The gene discussed is SAMD3; the disease is Hepatic fibrosis.