Based on findings that the TLR4/MyD88/NF-κB signaling pathway plays an important role in mediating inflammatory response and that EA can inhibit inflammatory response through the NF-κB signaling pathway, we speculate that EA may inhibit intracerebral inflammatory response through the TLR4/MyD88/NF-κB signaling pathway, thereby improving the cognitive dysfunction in HE. Here, TLR4 is linked to hereditary elliptocytosis.