In a study that used an ischemia-reperfusion mouse model to study FGF2 deficiency, cardiac-specific overexpression of all four isoforms of human FGF2, and wild-type mice, demonstrated significantly higher recovery in post-ischemic function and reduced infarction size in mice with overexpressed FGF2, providing evidence that endogenous FGF2 plays a significant cardioprotective role against ischemia-reperfusion injury [52] (Figure 1). The gene discussed is FGF2; the disease is infarction.