Since α-synuclein is overexpressed under certain pathological conditions of PD52,53 and these upregulated proteins can interfere with many physiological processes, such as ER-to-Golgi transport54, synaptic transmission55, and mitochondria function and morphology56, robustly knocking down the overexpressed α-synuclein using the Tat-βsyn-degron peptide may have better neuroprotective efficacy in restoring normal cellular functions in the PD brain than simply inhibiting the formation of toxic α-synuclein oligomers using the Tat-βsyn peptide. This evidence concerns the gene TAT and Parkinson disease.