CNR1 and steatosis: Accordingly, these findings suggest that, by activating hepatic CB1R, chronic alcohol intake stimulates the secretion of 2-AG by activated HSCs, which, in turn, promotes hepatic lipogenesis, on the one hand, and, on the other hand, inhibits fatty acid oxidation, thereby creating a disbalance between lipogenesis and lipid oxidation and resulting in chronic fat accumulation in the liver and steatosis [4,71,72,73].