Weirather et al., 2014 could show that depletion of Treg in a post-myocardial infarction model led to an inhibited production of anti-inflammatory factors essential for wound healing, like IL-10 and TGF-β1, an increased infiltration of neutrophils and monocytes, and an induction of “M1-like” macrophages [36]. This evidence concerns the gene TGFB1 and myocardial infarction.