Since it has been well documented that high levels of cholesterol and FFAs play a key role in the hepatic inflammation and the progression of NAFLD from hepatic steatosis to NASH [33, 34, 48, 49], it is obvious that LDLR-deficient mice are a better model than C57BL/6 mice in the investigation of pathogenesis of hyperlipidemia-associated NASH. This evidence concerns the gene LDLR and metabolic dysfunction-associated steatotic liver disease.