In addition, under ischemic stroke, ATP is released from damaged neurons or glia cells of infarct core region to extracellular space invoking peri-infarct astroglial and microglial/macrophage membrane P2 purinoceptors signaling, promoting the nucleus translocation of NF-κB-p65 to induce pro-inflammatory cytokine transcription and secretion, which is likely to initiate or aggravate motor and cognitive impairment [8, 13, 14]. Here, NFKB1 is linked to ischemic stroke.