In the context of PD, iPSC-derived BMECs from a preclinical patient carrying compound heterozygous loss-of-function mutations in PARK2 associated with familial early-onset PD failed to show active P-glycoprotein in apical-to-basolateral transport assays, which may indicate that patients with familial PD mutations are predisposed to loss of P-glycoprotein function [114]. Here, PRKN is linked to Parkinson disease.