Combined with others' reports showing that NLRP3 inflammasome activation plays a central role in the induction of inflammation and fibrosis in various liver pathologies such as nonalcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH) [26], and IL-1 participates in both the early fibrogenesis and the later maintenance of fibrosis in liver [10], these data suggest that targeting inflammasome activation related signaling pathways may represent an appealing strategy to ameliorate cholestatic liver fibrosis. Here, IL1B is linked to alcoholic fatty liver disease.