Conversely, VSIG deficiency leads to reduced M2 polarization and reduced production of IL10 and TGFβ in the MI hearts and in macrophage–fibroblast co-cultures, which is associated with impaired fibroblast pro-repair activities (compromised proliferation and, in that case, also collagen production and αSMA induction), leading to dysfunction and increased mortality due to MI rupture [134]. This evidence concerns the gene TGFB1 and myocardial infarction.