,59 TGF-β expression up-regulation and increased signaling activation were described in the context of elevation of gut-derived endotoxins, increases in oxidative stress, and accumulation of ethanol metabolites, such as acetaldehyde and lipid oxidation products, all as prerequisites of hepatocellular damage, as well as HSC and KC activation.60, 61, 62 Its up-regulation was also consistently found in advanced fibrosis and cirrhosis of patients with ALD.2 The gene discussed is TGFB1; the disease is Cirrhosis.