For that purpose, we treated cocultures of iNs and iAs with BFA1, to inhibit autophagy (mimicking a major lysosomal impairment), or CBE to inhibit GCase activity (mimicking Gaucher disease), both promoting lysosomal dysfunction and subsequent α-synuclein accumulation (Cleeter et al., 2013). The gene discussed is SNCA; the disease is Gaucher disease.