Conversely, α-syn aggregation in itself (e.g., without GBA1 mutations) induces GCase loss-of-function, and indeed GCase deficiency has been found in the brain, cerebrospinal fluid and blood of patients suffering from idiopathic PD [3,12,13], such GCase deficiency correlating with an increased α-syn burden. The gene discussed is GBA1; the disease is hyperinsulinemic hypoglycemia, familial, 4.