As MMP activities increase following MI, intracoronary- and MMP-degradable hydrogel-mediated supplementation of TIMP3 protein suppressed the activation of fibroblasts and cardiac fibrosis in pig ischemia/reperfusion (I/R) or MI models, and improved cardiac function in both models (Table 1) (Barlow et al., 2017; Purcell et al., 2018). The gene discussed is TIMP3; the disease is myocardial infarction.