These findings confirm that IL-17A contributes to liver fibrosis through two primary pathways: (1) IL-17A expressed in the liver interstitium directly activates HSCs to produce large amounts of collagen; (2) IL-17A stimulates endothelial cells and fibroblasts to secrete various cytokines, chemokines, and cell adhesion factors, inhibited ECM degradation, and promotes fibroblasts proliferation. This evidence concerns the gene IL17A and Hepatic fibrosis.