On the other hand, experimental studies performed in FABP4-deficient mice showed a decline in oxidative stress during myocardial ischemia/reperfusion (MI/R) injury and diabetes-induced cardiac dysfunction, as revealed by concomitant activation of the endothelial nitric oxide synthase/nitric oxide (eNOS/NO) pathway and reduced superoxide anion production [35]. The gene discussed is FABP4; the disease is diabetes mellitus.