Since A20 expression was mainly upregulated in cortical neurons in the ischemic/reperfusion area and there was a close relationship between A20 and NF-kB signaling, this suggests that A20-expresssing neurons may be the main target through which EA inhibits the inflammatory response after acute cerebral ischemia by regulating the neuronal NF-kB signaling pathway. Here, NFKB1 is linked to brain ischemia.