mRNA and protein levels of TGF-β1 are increased in myocardial-infarction scars and correlate with increased expression of collagen I and Smad3 phosphorylation, suggesting that activation of the TGF-β1/Smad3 signaling pathway may contribute significantly to myocardial fibrosis [24]. This evidence concerns the gene SMAD3 and myocardial infarction.