Moreover, neutralization experiments using gene therapy with the extracellular domain of the type II TGF-β receptor in a model of MI suggested that early inhibition may worsen dysfunction, accentuating the inflammatory response, while late disruption of TGF-β signaling may protect from interstitial fibrosis and hypertrophic remodeling (Prabhu and Frangogiannis, 2016). Here, TGFB1 is linked to myocardial infarction.