Previously, our group found that ApoC3 deficiency generated favorable lipoprotein profiles, then protecting against diet-induced atherosclerosis in hamster (9); however, whether ApoC3 inhibition still executed long-term beneficial function in atherosclerosis, a major event in FH with hypercholesterolemia due to lacking LDLR. The gene discussed is LDLR; the disease is familial hyperaldosteronism.