It is appreciated that the immune-mediated response in NASH involves both adipocytokines and increased intestinal permeability owing to gut dysbiosis; translocation of bacterial endotoxins will ensue, initially triggering the intrahepatic proinflammatory cascade of toll-like receptor 4 (TLR4) in the liver, and eventually culminating in the activation of hepatic stellate cells and signals converging toward a fibrotic phenotype owing to the chronic inflammatory activation of the liver-resident cells, as well as the necrotic and apoptotic pathways [118]. This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatohepatitis.