Early research in the field of atherosclerosis proved that macrophage-derived tumor necrosis factor-α (TNF-α) targets the structural domain of FAP, resulting in dose-dependent upregulation of FAP expression (34), while several in vitro experiments in myocardial infarction and oncology have demonstrated that FAP can be induced by transforming growth factor-β (TGF-β) through the classical drosophila mothers against decapentaplegic protein (SMAD) family member 2/3 pathway (35, 36). Here, TNF is linked to myocardial infarction.