LDLR and familial hyperaldosteronism: Although LDLR-deficient mice, especially homozygous animals, have been widely used for human atherosclerosis, accumulated data have demonstrated that they cannot replicate FH traits and are not suitable for the translational study of lipid disorder-related CHD, because heterozygotes are completely healthy and homozygotes exhibit mildly elevated cholesterol levels on regular chow diet [9].