The knowledge acquired from the protein products of identified causal genes and risk factors of PD and APS indicates that defects in vesicular transport pathways, endo-lysosomal dysfunction, impaired autophagy-lysosomal protein and organelle degradation pathways, α-synuclein aggregation and mitochondrial dysfunction play key roles in PD pathogenesis [2, 29, 121, 236, 371]. This evidence concerns the gene SNCA and autoimmune polyendocrinopathy.