It has been shown that the deficiency of MCP-1 in LDLR−/− mice leads to a significant reduction of the atherosclerotic lesions.[8] In accordance with the findings obtained in animal models, we in the present study demonstrated that MCP-1 was significantly increased in CAD patients, which revealed that an abnormal MCP-1 expression in CAD patients may contribute to the pathogenesis of atherosclerosis and CAD. Here, CCL2 is linked to atherosclerosis.