Increasing evidence shows that TGF-β1/TβR/Smad signaling pathway is regarded as a potential antifibrosis target against hepatic fibrosis induced by CCl4: TGF-β1, TβRI, TβRII, Smad2, and Smad3 are highly up-regulated in the form of either transcript or protein in the fibrotic tissues of animal models or human samples, while the expression of smad7 is decreased. The gene discussed is TGFBR2; the disease is Hepatic fibrosis.