The current research validated the advantageous function of TEAS during the initial stage after I/R and examined the neuroprotective mechanisms of TEAS (including reducing neuronal inflammation, apoptosis, and pyroptosis, as well as suppressing microglia activation) through the TLR4/MyD88/NF-κB pathway after ischemic stroke. The gene discussed is TLR4; the disease is ischemic stroke.