In an atherosclerosis model (on an ApoE-deficient background and after feeding a high-fat/cholesterol diet), we had found previously that endothelial inflammatory activation resulted in an accelerated and aggravated development of atherosclerosis, which was characterized by a significant inflammatory profile of the aortic transcriptome and a cellular transition of smooth muscle cells towards a non-contractile, synthetic phenotype and further on towards macrophage-like cells [14]. This evidence concerns the gene APOE and atherosclerosis.