In cellular models of PD, RTP801 shRNAs protected both sympathetic neurons and neuronal PC12 cells from neurotoxins.19 RTP801 knockdown also has been successful in treating ocular diseases like macular degeneration.50 Pharmacologically, rapamycin, by partially inhibiting mTOR, interferes with RTP801 translation and is protective in cellular and animal models of PD.23 Our data indicate that parkin contributes to decreasing cellular RTP801 protein levels. Here, PRKN is linked to macular degeneration.