Mechanistic studies on the clinical efficacy of CPYJT in the treatment of TS have been carried out previously on the content levels of monoamine neurotransmitters (DA, 5-HT, NE) in brain tissues and plasma [11, 12], the expression levels of DA transporters, the expression levels of DA receptors, and the changes of DA in the process of synaptic vesicle release, as well as the effect of blood-brain barrier permeability. The gene discussed is SLC6A3; the disease is Timothy syndrome.