Autophagy can exert either beneficial or detrimental effects on cerebral ischemic injuries, as moderate autophagy may help degrade aggregated proteins,144–146 whereas inadequate or excessive autophagy may eventually lead to cell death.147 The dual role of autophagy in ischemic stroke may be explained by the involvement of multiple signaling pathways, such as mammalian target of rapamycin (mTOR), 5′-AMP-activated protein kinase (AMPK), MAPK, NF-κB, p53, HIF-1, and Bcl2 pathways.148. The gene discussed is TP53; the disease is ischemic stroke.