To elucidate the molecular mechanism of cardiac fibrosis after acute myocardial infarction (AMI) regarding miR-208b/miR-21 via the TGF-β1/Smad-3 signaling pathway, we detected the expression levels of miR-208b/miR-21 and TGF-β1/Smad-3 in cells and blood samples from AMI patients and analyzed their relationships. This evidence concerns the gene SMAD3 and acute myocardial infarction.