Inflammatory signaling and oxidative stress are two major components in the pathogenesis of alcoholic he-patitis.Alcohol consumption results in translocation of gut bacteria into the portal system along with lipopolysaccharides that interact with toll-like receptors and results in the production of inflammatory and immunogenic mediators such as tumor necrosis factor-alpha(TNF-α) and interferons.Chronic consumption of alcohol causes priming of this process in which there is enhanced production of cytokines,interferon,interleukins,and TNF-α.Oxidative stress,genetic predisposition,and the unfolded protein response are other contributory mechanisms.Novel therapies aimed at these pathways may prevent,decrease,or delay the complications of alcoholic hepatitis.