We could observe that the loss of GCase activity and the presence of mutant forms of the GBA protein was clearly associated with an increase in different neurotoxic forms of α-syn associated with PD, including oligomeric, insoluble, phosphorylated and extracellular species (Fig. 3a–e); the aim of this work was to identify underlying pathways leading to α-syn accumulation in our GBA in vitro model. This evidence concerns the gene GBA1 and Parkinson disease.