The combined inhibition of three chemokine–receptor systems, MCP-1 (CCL2)/CCR2, fractalkine (CX3CL1)/CX3CR1, and CCL5/CCR5, was reported to abolish development of atherosclerosis in an Apoe−/− mouse model [110], supporting nonredundancy of these chemokines with regard to monocyte mobilisation in atherosclerosis. Here, CCL2 is linked to atherosclerosis.