In the case of intracellular cholesterol overload, SREBP-2, one of the main nuclear factors regulating cholesterol metabolism, is abnormally activated under the action of proinflammatory factors, resulting in the increased expression and activity of LDL receptor (LDLR) and HMGCR, which in turn results in excessive accumulation of cholesterol in the liver, accelerating the development of fatty liver disease [54]. The gene discussed is LDLR; the disease is fatty liver disease.