Several typical pathological features of alcohol-induced liver damage (observed in EtOH-fed WT mice) such as liver inflammation, DR, cholestasis, biliary and hepatocyte senescence, liver angiogenesis, steatosis, and fibrosis were ameliorated in Sct−/− mice demonstrating an impactful relationship between Sct stimulation and the subsequent onset of pathological features after EtOH exposure. The gene discussed is SCT; the disease is cholestasis.