As a central event in the development of hepatic fibrosis, HSCs are activated by liver injury, usually with changes in gene expression and major phenotypical transformation to α-smooth muscle actin (α-SMA)-positive myofibroblasts that increase malignant biological characteristics [17], produce large amounts of collagen and other ECM molecules [18], and secrete proinflammatory cytokines such as tumor necrosis factor- (TNF-) α and interleukin- (IL-) 1β [19]. Here, ACTA1 is linked to Hepatic fibrosis.