Cell death after cerebral ischemia was considered to be exclusively necrotic in nature, but research over the past decade has revealed that after a stroke, many neurons in the ischemic penumbra undergo apoptosis.51 To characterize apoptosis caused by glutamate-induced excitotoxicity, we confirmed the effect on increased intracellular calcium levels, mitochondrial membrane potential and the proapoptotic proteins caspase 3 and AIF.52 Consistent with their antioxidant effects, both MK-X and EPO decreased activation of the apoptotic cascade after induction of excitotoxicity. The gene discussed is EPO; the disease is Stroke.