Increased expression of human FGF2 has been shown to reduce postischemic cardiac dysfunction and myocardial infarct size through activation of protein kinase C (PKC), mitogen‐activated protein kinase (MAPK), and nitric oxide signaling (House et al. 2005, 2007; Manning et al. 2012). This evidence concerns the gene PRRT2 and myocardial infarction.