Mutations found in genes encoding α-synuclein [2], parkin [3], PTEN-induced putative kinase 1 (PINK1) [4], DJ-1 [5], Leucine-rich repeat kinase 2 (LRRK2) [6], and VSP35 [7], [8] are known to play roles in rare familial forms of PD, indicating that protein misfolding and aggregation, defects in the ubiquitin-proteasome system (UPS), mitochondrial dysfunction and cellular signaling are among other mechanisms involved in the pathogenesis of PD. This evidence concerns the gene LRRK2 and Parkinson disease.