The combined blocking of CCL2 and the receptors CX3CR1 and CCR5 markedly attenuated bone-marrow monocytosis and reduced circulating monocyte numbers, which correlated with a substantially reduced accumulation of macrophages within atherosclerotic lesions [31]; thus, CCL2, CX3CR1, and CCR5 appear to play an additive and independent role during atherosclerosis, indicating that chemokines might regulate various processes of the accumulation of monocyte-derived macrophages within atherosclerotic lesions [31]. The gene discussed is CX3CR1; the disease is atherosclerosis.