EA can achieve this kind of intervention (in animal ischemic models) via the inhibition of NF-kB-mediated neuronal cell apoptosis, reducing autophagy, modulating p38, ERK1⁄2, and JNK, and downregulating the expression of Nogo-A and NgR in the hippocampus of the cerebral ischemia side, thus reducing cerebral infarct volumes with improvements in neurological deficit motor and cognitive scores [80]. Here, NFKB1 is linked to infarction.