The pathogenic role of autophagy in PD was revealed by increasing levels of α-synuclein when lysosomes are inhibited, and misfolded α-synuclein oligomers can be removed by different catabolic pathways including macroautophagy and chaperone-mediated autophagy (CMA) with different pathological situations, while α-synuclein monomers are also degraded by the proteasome [121, 122], suggesting a close link between α-synuclein degradation and autophagy. The gene discussed is SNCA; the disease is Parkinson disease.