Because the development of significant atherosclerotic lesions in mice requires a hyperlipidemia background, we have bred each of the strains to a common strain (C57BL/6J) that donated transgenes for two dyslipidemia-inducing mutations: human apolipoprotein E-Leiden (APOE-Leiden) and human cholesteryl ester transfer protein (CETP). This evidence concerns the gene APOE and metabolic syndrome.