Although it has been known that EA pretreatment can induce significant tolerance to ischemic brain injury [13,39-42] and inhibit inflammatory responses, such as activation of NF-κB and proinflammatory cytokine generation [21,40], the molecular mechanisms that contribute to brain ischemia tolerance by EA pretreatment are not well understood. The gene discussed is NFKB1; the disease is brain ischemia.