In mice, hypercholesterolemia and atherosclerosis can be observed when genetically engineered mouse models with deficient clearance of apoB-containing lipoproteins such as Apoe-deficient mice (Apoe−/−) or Ldlr-deficient mice (Ldlr−/−) are fed a western diet (high saturated fatty acids, high CS) [5]. The gene discussed is LDLR; the disease is familial hypercholesterolemia.