Moreover, the infiltration of macrophages, release of pro‐inflammatory cytokines (IL‐1, IL‐6, TNF‐α, and MCP‐1) and superoxide levels are up‐regulated in Ang II‐induced mouse AF models, which may promote the development of fibrosis and the related structural and electrical remodelling of AF.5, 6. This evidence concerns the gene CCL2 and atrial fibrillation.