A limitation of our studies is the fact that we have used total Sct−/− mouse ALD models that do not exclude the possibility that changes in hepatic steatosis may be due to impaired intestinal lipid absorption; however, we have developed a cholangiocyte-specific SR−/− mouse model that we will use in future experiments to pinpoint the role of biliary Sct/SR signaling on liver phenotypes [43]. The gene discussed is SCT; the disease is Hepatic steatosis.