Our data further suggest that the elevated levels of cardiac iNOS in hyperhomocysteinemic mice are protective against oxidative stress and I/R injury, because Nos2−/− mice had increased cardiac ROS production (Figure 6C) and increased infarct size (Figure 5) compared with Nos2+/+ mice in the setting of hyperhomocysteinemia. The gene discussed is NOS2; the disease is hyperhomocysteinemia.