PRKN and Parkinson disease: Altogether, when assessing mitochondrial function in the hiPSC-derived DA neuron model, we were able not only to confirm an impaired mitochondrial phenotype observed previously in hiPSC-derived DA neurons of homozygous PRKN-PD patients, but also to observe changes in mitochondrial homeostasis in clinically unaffected individuals carrying a heterozygous variant in PRKN, although these data need further confirmation since they are based on only two variant carriers.