Highlighting the role of lysosomal dysfunction in the pathogenesis of PD, results from postmortem brain tissue and IPS cell-derived neurons show that reduced lysosomal GCase activity is paralleled by increased levels of alpha-synuclein, not only in PDGBA but, to a lesser degree, also in cases with PDGBA_wild type (Gegg et al., 2012; Murphy et al., 2014; Schondorf et al., 2014; Moors et al., 2019). This evidence concerns the gene SNCA and Parkinson disease.