In the ApoE−/− mouse model, inhibition of three pathways, including CCL2, CX3CR1, and CCR5, almost abrogates macrophage accumulation and atherosclerosis (90% reduction), which is significantly more than the 28%, 36%, or 48% reduction in ApoE−/− CCL2−/−, ApoE−/− CX3CR1−/−, and ApoE−/− CCL2−/− CX3CR1−/− murine models, respectively [50]. This evidence concerns the gene CX3CR1 and atherosclerosis.