Studies have suggested that promoting hepatic cell repair through the prevention of apoptosis in the diseased liver by targeting death effectors, such as Fas or its downstream caspases, is a viable strategy for curtailing the progression of ESLD, such as viral hepatitis, NAFLD, alcoholic steatohepatitis, drug abuse, and autoimmune diseases [28, 29]. This evidence concerns the gene FAS and alcoholic fatty liver disease.