Increasing lysosomal GCase, thereby decreasing αS oligomer formation, disrupts this pathogenic loop.87 By way of follow-up, the same group found that increasing lysosomal GCase activity in iPSC-derived dopamine neurons from patients with PD-associated GBA mutations reduced αS accumulation.100 In keeping with this concept, a study of the impact of GBA deficiency on αS homeostasis found that glycosphingolipid accumulation resulting from GBA loss-of-function decreased physiological αS multimers and increased the more aggregation-prone monomeric form. The gene discussed is GBA1; the disease is Parkinson disease.