Promoting the activation of HSCs and pathogenesis of hepatic fibrosisvia TLR4 and TGF-β/SMADs signaling pathway[90].Promoting the production of IL-6 in mouse biliary epithelial cells through TLR2-mediated protein kinase B (AKT) and p38 pathways, resulting in the aggravation of hepatic fibrosis in mice[91].Promoting the progression of CCA through the interaction between normal cholangiocytes and CCA cells, mediated by extracellular signal-regulated kinase 1/2/NF-κB/matrix metalloproteinase-9 and integrin β4-focal adhesion kinase/steroid receptor coactivator[93–94]. This evidence concerns the gene MAPK3 and hepatitis A virus infection.