Among others, reduced enzymatic activity of glucocerebrosidase and its complex interplay with α-synuclein pathology, alterations in the autophagy-lysosomal pathway (ALP), unfolded protein response (UPR), and endoplasmic reticulum (ER) stress have been implicated in GBA1-PD pathogenesis [12]. This evidence concerns the gene GBA1 and Parkinson disease.