The activation of pro-apoptotic p53 and Fas ligand (CD95/Apo1)-mediated pathways, a decrease in the Nrf2 antioxidant cascade, malfunctioning of the ubiquitin-proteasome system (UPS), and inhibition of the mitogen-activated protein kinase (MAPK) signaling pathway are observed in Gpx1 knockout (KO) mice after ischemic stroke. The gene discussed is GPX1; the disease is ischemic stroke.