Recent reports suggest that the recruitment of inflammatory monocytes (Ly6ChighCCR2+ in mice, CD14highCD16− in humans) contributes to myocardial inflammation after MI6, 7, 8, and endogenous angiotensin II and monocyte chemotactic protein-1 (MCP-1), a ligand for CCR2, play important roles in this process, suggesting their roles as potential therapeutic targets for IR injury9, 10, 11. This evidence concerns the gene CCL2 and inflammation.