Whilst we understand from prior studies that atherosclerosis develops due to the infiltration of monocytes and T cells into the vessel wall [39], the mechanism for its cellular attraction has recently been proven by demonstrating that CX3CR1 gene-deleted apoE-/- mice had a significant reduction in macrophage infiltration towards the vessel wall as compared to apoE-/- mice with an intact CX3CR1 gene, when both murine groups were fed with a high-fat diet [40]. This evidence concerns the gene APOE and atherosclerosis.