Over the past decade, several putative mechanisms of α-synuclein accumulation in individuals both with idiopathic PD and PD-GBA1 have been proposed, including lysosomal and mitochondrial dysfunction, endoplasmic reticulum stress, and impaired lipid metabolism, protein trafficking and α-synuclein clearance [3,23,24]. This evidence concerns the gene GBA1 and Parkinson disease.