In particular, low-density lipoprotein receptor deficient (LDLR−/−) mice, an established diet-induced model of both NAFLD and atherosclerosis, which are susceptible to diet-induced hepatic inflammation and fibrosis, which can lead to the progression of simple steatosis to NASH and the development of atherosclerosis, were fed a western-type diet and treated with a pharmacological inhibitor of sphingolipid biosynthesis [197]. The gene discussed is LDLR; the disease is atherosclerosis.