Although PPARγ is expressed mainly in macrophages and induces β-oxidation of fatty acids, pan-PPAR agonists that target all PPAR isoforms have been reported to drive hepatic macrophages to acquire an anti-inflammatory phenotype and ameliorate liver fibrosis in experimental models of nonalcoholic steatohepatitis (NASH) (induced by diet) and chronic toxic injury (via chronic CCl4 administration) [80, 81]. This evidence concerns the gene PPARA and Hepatic fibrosis.