ACTA1 and Hepatic fibrosis: There are numbers of risk factors, such as chronic hepatitis virus, S. japonicum-infection and alcohol consumptions, that could activate quiescent HSCs into activated HSCs, which then transform into proliferative, fibrogenic, proinflammatory, and contractile myofibroblasts, and produce α‐SMA and collagen, further contributing to the development of liver fibrosis (33, 34).