It has been shown that heterozygous LDLR-deficient (Ldlr+/−) hamsters exhibit significant dyslipidemia similar to that observed in human subjects with familial hypercholesterolemia (FH) [96], thus serving as an ideal animal model for experimental investigations of FH and related conditions such as atherosclerosis-related coronary heart disease [97,98]. The gene discussed is LDLR; the disease is familial hyperaldosteronism.