In an attempt to explore the role of Siglec-9/E in atherosclerosis, we generated apoE/Siglec-E double deficient (apoE−/−/SE−/−) mice to assess the effect of Siglec-E deletion on apoE−/− mice, which is a mouse model developing hypercholesterolemia and atherosclerotic lesions similar to those in humans [10]. This evidence concerns the gene APOE and atherosclerosis.