In clinical treatment, experimental studies have shown that hyperbaric oxygen can reduce the production of free radicals after intracerebral hemorrhage by regulating SOD levels, inhibit the excessive production of NO after cerebral hemorrhage, and enhance ATPase activity, thereby further reducing the occurrence of cerebral edema (Wada et al., 2000; Narkowicz et al., 1993). The gene discussed is SOD1; the disease is intracerebral hemorrhage.