Afterwards, during the reparative phase post‐MI, macrophages in the infarcted myocardium dominantly shift from M1 into M2 phenotype producing anti‐inflammatory/reparative cytokines, such as TGF‐β, VEGF and IL‐10, which tune the anti‐inflammatory and reparative response and facilitate wound repair by activation of myofibroblasts, angiogenesis and the ECM deposition.62, 63, 64, 65. This evidence concerns the gene IL10 and myocardial infarction.