Based on the emerging links between GBA1 genotype and αS biology and on the previous success in reestablishing αS tetramers and normalizing phenotypes when inhibiting SCD, we applied a SCD inhibitor to GBA-PD patient-derived neurons and knock-in (KI) mice with decreased GCase activity and αS aggregation pathologies (50–54). This evidence concerns the gene GBA1 and Parkinson disease.