EA at Hegu (LI4) and Taichong (LR3) can regulate the content of neurotransmitters (upregulating 5-HT and GABA, downregulating Glu levels), upregulate the expression of synapse-associated proteins such as Syn and PSD-95, activate the brain-derived neurotrophic factor (BDNF)/tyrosine-protein kinase B (TrKB)/cAMP response element binding protein (CREB) signaling pathways, ameliorate morphological abnormalities and preserve synaptic ultrastructure of neural cells in the hippocampus of rats, finally alleviate spinal hyperreflexia and motor dysfunction (Yang P. et al., 2023). The gene discussed is BDNF; the disease is Hyperreflexia.