Patients with advanced hepatitis C virus-induced fibrosis or nonalcoholic steatohepatitis, as well as animal models of liver fibrosis induced by carbon tetrachloride (CCl4) and thioacetamide (TAA), have increased intrahepatic levels of CXCL4 suggesting a role of CXCL4 in the fibrogenic process. This evidence concerns the gene PF4 and metabolic dysfunction-associated steatohepatitis.