Prolonged IL‐2 signaling promotes terminal‐effector differentiation in vivo.43 IL‐2 levels are elevated in serum samples from stroke patients taken 24 hours after stroke onset and are sustained in severe patients.30 Daclizumab, a humanized monoclonal antibody directed against high‐affinity IL‐2R and modulates IL‐2 signaling, shows a high efficacy in reducing immune pathogenesis of MS.44 Therefore, neutralizing IL‐2 after stroke is likely to block the activation of CD8+ T cells and protects against demyelinating injuries after stroke. The gene discussed is CD8A; the disease is Stroke.