Mitochondrial dysfunction is an important pathological element mediating the onset of neurodegenerative disorders (e.g., PARK2 mutations are associated with increased ROS and mitochondrial dysfunction in patients with Parkinson disease), and previous work in mouse models suggests that Park2-deficient photoreceptors exhibit ectopic mitochondria localization upon light exposure, thus suggesting that aberrant trafficking of damaged mitochondria might be one of the mechanistic aspects of retinal degeneration [55]. The gene discussed is PRKN; the disease is retinal degeneration.