CCR2 is a chemokine receptor that binds monocyte chemoattractant proteins (MCP-1, 2, 3 and 4). Two spliced variants were initially described for CCR2 (CCR2A and CCR2B). These variants differ in their terminal carboxyl tails (1). Monocyte adhesion to the arterial endothelium and subsequent migration into the intima are central events in the pathogenesis of atherosclerosis. CCR2 and MCP-1 has been associated to atheroscletotic plaques (2, 3). MCP-1 is induced by modified-LDL in endothelial cells, and may trigger firm adhesion of monocytes to vascular endothelium under flow. Local overexpression of MCP-1 at vessel wall induces infiltration of macrophages and formation of atherosclerotic lesion (4). Absence of MCP-1 reduces the lesion size in MCP-1−/− apoE−/− mice in the apoE gene deleted mouse atherosclerosis model (5, 6). Obesity induces an inflammation state that is implicated in many clinically important complications, including insulin resistance, diabetes, atherosclerosis and non-alcoholic fatty liver disease. CCR2 influences the development of obesity and associated adipose tissue inflammation (7).