Nevertheless, the present data suggest that augmentation of immunoproteasome may be involved in regulating inflammation cytokines production via regulating activation of NF-κB in ischemia stroke whereas selective inhibition of the immunoproteasome subunit affords a strong reduction of infarction volumes and a suppression of proinflammatory cytokines after MCAO, indicating that immunoproteasome-specific inhibitor might be an effective anti-inflammation agent for stroke treatment. The gene discussed is NFKB1; the disease is infarction.