Many new mechanisms for alcoholic steatosis have been suggested by work reported in the last 5 years. These include alterations of transcriptional controls of lipid metabolism, better understanding of the effects of abnormal methionine metabolism on the endoplasmic reticulum (ER) stress response, unraveling of the basis for sensitization of the Kupffer cell to lipopolysaccharide (LPS), a better understanding of the role of cytokines and adipokines in alcoholic liver disease, and implication of the innate immune and complement systems in responses to alcohol. Much of this work has been facilitated by work with knockout mice. Undoubtedly there are interrelationships between these various pathogenic mechanisms which ultimately will provide a more cohesive picture of how heavy alcohol use deranges hepatic lipid metabolism.