As mentioned above, reactive DA quinones, which are generated via spontaneous oxidation of cytosolic free DA outside the synaptic vesicle in DA neurons, can covalently react with the sulfhydryl residues on functional proteins, e.g., tyrosine hydroxylase (TH), DA transporter, and parkin, to cause the dysfunction of these proteins by forming quinoproteins in the pathogenesis of PD [14,15,16]. This evidence concerns the gene TH and Parkinson disease.