Although manipulation of specific genes reported in familial PD, including transgenic overexpression for α-synuclein and leucine-rich repeat kinase 2 and knockout models for Parkin, DJ-1, phosphatase, and tensin homolog-induced novel kinase 1, made it possible to establish many mouse models, none of them recapitulate key clinical and neuropathological features of PD entirely, especially in the absence of neurodegeneration of dopaminergic neurons (Dawson et al., 2010). Here, SNCA is linked to Parkinson disease.