PRKN and hyperinsulinemic hypoglycemia, familial, 4: To determine whether mitochondrial function was mechanistically linked to the differential phenotypic expression of Parkin deficiency, we measured mitochondrial energy production, membrane potential (ΔψM), oxygen consumption rate (OCR), and vulnerability to a mitochondrial complex I inhibitor rotenone33 in patient-derived cell lines from both the asymptomatic carrier and Parkin MT1 who is an affected family member of the asymptomatic carrier.