Since then, cholesterol-fed rabbits along with Watanabe heritable hyperlipidemic (WHHL) rabbits, a mutant rabbit with genetic deficiency of LDL receptor functions, have been extensively used to elucidate multiple facets of the pathophysiology of human atherosclerosis, leading to the discovery of the LDL receptor functions in familial hypercholesterolemia (Goldstein et al., 1983) and the development of the most-prescribed lipid-lowering drug, statin (Brown and Goldstein, 2004). This evidence concerns the gene LDLR and atherosclerosis.