Earlier, we found differences in lysosomal hydrolase activity (alpha-galactosidase (GLA), alpha-iduronidase (IDUA)) in iPCS neurons of GBA-PD compared to GBA carriers, suggesting that a more pronounced imbalance of sphingolipid metabolism may lead to impaired lysosomal clearance and launch the diseases associated with GCase deficiency [67]. This evidence concerns the gene GBA1 and hyperinsulinemic hypoglycemia, familial, 4.