In this study, we crossed ApoC3-deficient hamsters with a background of LDLR deficiency to generate a double knockout (DKO) hamster model (LDLR−/− XApoC3−/−, DKO) and investigated the role of ApoC3 inhibition in lipid metabolism and atherosclerosis in the hamster model of FH. This evidence concerns the gene APOC3 and familial hyperaldosteronism.