Our study introduces the concept that, in addition to the direct effects of EtOH on hepatocyte functions [42], alcohol feeding induces changes in Sct-dependent biliary phenotypes which contributes to liver fibrosis and lipogenesis and subsequently hepatocyte steatosis which is in keeping with our previous study in animal models of NAFLD (29). The gene discussed is SCT; the disease is metabolic dysfunction-associated steatotic liver disease.