Plasma, sera, CSF, and blood-derived MOs of PD patients with GBA mutations have shown partial GCase deficiency and its impact on the higher production of pro-inflammatory cytokines (e.g., IFNγ, TNFα, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-13, CCL2, CCL3, CCL18, and SF), midbrain damage, and cognitive defects (Table 3B). The gene discussed is GBA1; the disease is Parkinson disease.