As we continue to delineate the mechanism, it seems increasingly evident that α-synuclein is at the center of propagation of PD pathogenesis, whether that be through affecting mitochondria function (through import and association with the inner membrane, in turn affecting the activity of the electron transport chain and increasing the production of reactive oxygen species), cross-interactions with other pathways, such as TOR, or altering protein synthesis machinery. This evidence concerns the gene SNCA and Parkinson disease.