In human-derived cells, the contribution of Miro1 in lipid exchange and biosynthesis was confirmed by the discovery that patient-derived fibroblasts with PD-associated mutations in Miro1 displayed an altered formation of autophagosomes, which is dependent on the conversion of phosphatidylserine (PS) to phosphatidylethanolamine (PE) at MERCs (13, 14). The gene discussed is RHOT1; the disease is Parkinson disease.