Wu et al. found that AST could activate nuclear factor erythroid-related factor 2 and the antioxidant responsive element (Nrf2-ARE) pathway in subarachnoid hemorrhage model rats, resulting in upregulating cortical endogenous antioxidant levels, reducing oxidative damage, brain edema, and disruption of the blood-brain barrier (BBB), inhibiting apoptosis, as well as improving neurological function and ameliorating brain injury (Wu et al., 2014). The gene discussed is NFE2L2; the disease is subarachnoid hemorrhage.