Non-sterol ligands lack the biophysical properties to arrest Srebf1 maturation, and their administration is marked by hepatic steatosis and hypertriglyceridemia (Schultz et al., 2000; Grefhorst et al., 2002; Bradley et al., 2007; Kirchgessner et al., 2016). The gene discussed is SREBF1; the disease is fatty liver disease.