SMAD3 and Hepatic fibrosis: Elevated TGF-β/Smad3 pathway activity and reduced expression of miR-34a also contribute to liver fibrosis in HBV infection, whereas the over-expression of miR-34a in human hepatic stellate cells significantly attenuated fibrosis and TGF-β1/Smad3 activation by targeting Smad4 [228].