AA exhibited protective activity against experimental models of liver fibrosis by acting as regulatory factor on the PI3K/AKT/mTOR and Bcl-2/Bax signaling pathways; these mechanisms induced a clear prevention of the progression of liver fibrosis, as revealed by the assessment of liver fibrosis-related indexes (i.e., body weight, biochemical parameters, biomarkers, histological alterations, etc.)[110]. The gene discussed is BAX; the disease is Hepatic fibrosis.