Both ApoE−/− and LDLR−/− mice develop hypercholesterolemia; however, their lipoprotein profiles differ significantly.[24] ApoE−/− mice exhibit markedly elevated cholesterol concentrations carried in VLDL and chylomicron remnants, with minimal HDL cholesterol concentrations, even when fed normal laboratory diet.[19] In contrast, LDLR−/− mice develop hypercholesterolemia characterized by increased LDL cholesterol concentrations when fed a high-fat or Western diet.[19] These differences may influence the pathophysiology of AAAs, resulting in the alteration of AAA susceptibility in ApoE−/− mice. This evidence concerns the gene APOE and triple-A syndrome.