LDLR and familial hypercholesterolemia: Most commonly used atherosclerosis-prone mouse models are the apolipoprotein E-deficient (ApoE−/−) and LDL receptor-deficient (Ldlr−/−) mice, which exhibit a phenotype driven by extreme hypercholesterolemia that exceeds the level found in most patients with atherosclerosis and can act as the sole atherogenic factor that masks the potential effect of insulin resistance in the pathogenesis of atherosclerosis [5].