In subsequent experiments (64), MPTP-induced mice were still selected as the animal model, but the acupoints were changed to GV20 (Bai hui); GV29 (Yin Tang) treatment, and the results showed that EA regulated and activated downstream pathways (such as PI3K/ Akt and ERK1/2) via the TKB FL/TrkB T1 ratio to counteract MPTP-induced Parkinson’s disease in mice, and upregulated BDNF expression against the neurotoxicity of MPTP. The gene discussed is BDNF; the disease is Parkinson disease.