Loss-of-function mutations in the ubiquitin E3 ligase parkin are the most common cause of autosomal recessive Parkinson's disease (PD).1 Multiple functions have been ascribed to parkin, most notably the inhibition of apoptosis2, 3, 4, 5, 6, 7 and the induction of autophagic mitochondrial turnover (mitophagy).8, 9 However, the relative scale of these effects mediated by endogenous parkin and whether these processes can occur concomitantly or are mutually exclusive, is not known. Here, PRKN is linked to Parkinson disease.