In this study, we conclude that the overexpression of miR-29a under long-term HFD can improve hepatocellular steatosis and liver fibrosis, likely by targeting CD36 transcripts and subsequent events, including the reduction of fatty acid flux, the expression of inflammation, and the progression and fibrogenesis of EMT, thus providing a potential target for modulating NAFLD. The gene discussed is CD36; the disease is Hepatic fibrosis.