In addition, after myocardial infarction, NOD-like receptor pyrin domain-containing protein 3 (NLRP-3) inflammasome forms in cardiac fibroblasts, exacerbating damage to cardiac tissue and causing fibrosis via the TGF-beta/SMAD pathway, which can lead to reactive oxygen species and inflammasome accumulation (25). The gene discussed is NLRP3; the disease is myocardial infarction.