It was well accepted that inflammation promotes the development and perpetuation of AF.31 Pro‐inflammatory cytokine levels were elevated with heart failure induced by TAC.17 Therefore, to evaluate whether CYP2J2/EET counteracts the inflammatory response in AAC mice, we measured important pro‐inflammatory cytokines and chemokines including TNF‐α, IL‐6 and MCP‐1, and our data demonstrate the serum level of TNF‐α, IL‐6 and MCP‐1 were significantly increased in mice with AAC (Figure 5A). The gene discussed is CCL2; the disease is persistent truncus arteriosus.