The deficiency of MCP-1 can result in a significant reduction of atherosclerotic lesions in LDLR−/− mice.[8] Meanwhile, in patients at risk for developing atherosclerosis, serum MCP-1 level correlates with inflammatory activity.[9] Dewald et al[10] observed that inhibition of MCP-1 with a neutralizing antibody leads to a decreased and delayed macrophage infiltration in the healing infarct as well as a delayed replacement of dead cardiomyocytes with granulation tissue, therefore, attenuating left ventricular function. Here, CCL2 is linked to atherosclerosis.