In the acute myocardial infarction (AMI), model study showed that TGF-β1-induced transition of cardiofibroblasts into myofibroblast-like cells can be attenuated by the TG2 inhibitor 1–155, suggesting a new role for TG2 in regulating TGF-β1 signaling in addition to its role in latent TGF-β1 activation [53]. The gene discussed is TGM2; the disease is acute myocardial infarction.