There is evidence showing that Treg may play a role in suppression of the post-infarction inflammatory response [113]: following MI, Treg infiltrate the healing myocardium, where they induce the differentiation of M2 macrophages and secrete anti-inflammatory factors, like IL-10 and TGF-β, to inhibit the inflammatory response of M1 macrophages and lymphocytes, thereby ameliorating inflammation-mediated cardiac damage [112,114]. This evidence concerns the gene IL10 and myocardial infarction.