A major obstacle for mechanistic studies is that parkin-KO mice show minimal defects in striatal DA release and no loss of DA neurons in the SNpc, most probably due to compensation for parkin deficiency during development, because parkin KD (Fig. 7 and Supplementary Figs. 12 and 13) or conditional parkin-KO in the SNpc produced similar PD neurotoxicity in adult mice17,20,40,41. The gene discussed is PRKN; the disease is Parkinson disease.