In addition, endotoxemia resulting from hepatocellular and immune dysfunction and portosystemic shunt may contribute to impaired protein synthesis and potentially active autophagy via tumor necrosis factor-alpha (TNFα)-dependent and potentially TNF-independent pathways [19], such as reducing micronutrients derived from gut-microbiota (butyrate, acetate) [50]. This evidence concerns the gene TNF and serum lipopolysaccharide activity.