The phenotypic readouts of these effects is a reduction of the pro-atherogenic lipid profile and an attenuation of the tendency toward development of atherosclerotic plaques in ApoE−/− and LDLr−/− mice [16]–[17], two genetic models of dyslipidemia-driven atherosclerosis, as well as in rodents strains characterised by insulin resistance and liver steatosis [16]–[20]. Here, APOE is linked to metabolic syndrome.