TGF-β, however, was shown to promote disease and adverse cardiac remodelling during later stages of myocarditis: TGF-β-mediated Wnt secretion promoted myofibroblast differentiation and myocardial fibrosis in EAM [91], while treatments targeting TGF-β prevented fibrosis and heart failure [92–94]. This evidence concerns the gene TGFB1 and myocarditis.