CCL2, also known as MCP-1, is a member of the CC?β chemokine family. It is widely expressed in endothelial cells, smooth muscle cells, and monocytes in response to several atherogenic stimulants such as CD40 ligand, platelet derived growth factor (PDGF), interleukin-1β (IL-1β) and oxidized low density lipoprotein. Several recent in vivo studies have disclosed critical roles of MCP-1 in atherosclerosis. In addition, MCP-1 has been implicated in monocytic infiltration of tissues during several inflammatory diseases and has been implicated in macrophage-mediated tumor growth suppression in mice. CCL2 has been shown to have direct effects on tumor cells in an autocrine and paracrine fashion in multiple cancer types, including breast, lung, cervix, ovary, sarcoma, and prostate. In addition, MCP-1 plays a key role in the regulation of MMPs during transmigration. MCP-1 has been described as a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy. Kidney epithelial cells, including glomerular podocytes and tubular cells make MCP-1 in response to high glucose and advanced glycation end products. MCP-1 promotes inflammation and progressive injury in diabetic kidneys. The importance of MCP-1 in the early development of diabetic nephropathy has been determined ?in animal models incorporating genetically deficient mice or therapeutic blockade of MCP-1 receptor (CCR2).