Taken together, our findings suggest that expression of miR-125b is increased by TGF-β in activated HSCs, and the increased miR-125b binds to the 3′ UTR of Stard13 and inhibits its expression, thereby enhancing the RhoA/Mrtf-A/Srf signaling and leading to the increased expression of α-SMA and type I collagen and augmented contraction of HSCs, consequently resulting in hepatic fibrosis (Figure 7). The gene discussed is RHOA; the disease is Hepatic fibrosis.