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. This evidence concerns the gene NFKB1 and Stroke.