Timp3-deficiency exacerbates cardiac remodeling, dysfunction, and survival following MI (Figure 2), partly through increased MMP activity, TNF-α signaling, and apoptosis in the non-infarcted myocardium, while coronary density was not reduced in the myocardium (Tian et al., 2007; Kandalam et al., 2010). The gene discussed is TNF; the disease is myocardial infarction.