However, in vivo, despite the increased macrophage efflux from macrophages in APOE−/− APOC1+/+ mice, there was a robust +87% increase of the atherosclerotic lesion of the aortic root, as compared with APOE−/− APOC1−/−, a result that was attributed to the supplementary hyperlipidemia from both triglycerides and cholesterol [151]. This evidence concerns the gene APOC1 and hyperlipidemia.