Consistently with these studies, it was observed that the expression of TLR4/NF-κB was significantly decreased in the TNC in repeated IS-induced migraine-like models after EA treatment, which is consistent with the inhibition of microglia, and demonstrates that EA could improve the activation status associated with microglia by reducing TLR4/NF-κB. The gene discussed is NFKB1; the disease is migraine disorder.