The role of gut microbiota, along with the corresponding translocation of endotoxin into circulation, has been demonstrated for many diseases including Crohn’s Disease, ulcerative colitis, HIV and diabetes. A recent publication in the Journal of Clinical Gastroenterology has extended this to liver disease. Using several different mouse models to simulate liver disease, they found significant differences in the microbiome compared to healthy control mice. Several mechanisms for this link were explored, including an increase in gut permeability leading to an increase in circulating endotoxin. Given that Toll-like receptors are required for sensitivity to liver fibrosis, and the role that endotoxin plays in other inflammatory diseases, this is an especially attractive possibility.