The data presented here, along with those of two other recent reports (Delgado-Camprubi et al., 2016; Lehmann et al., 2016), indicate that the inhibition of PARPs could be a viable strategy to protect neurons from the neurotoxic consequences of mutations in genes encoding mitophagy components, such as PINK1, PARKIN and FBXO7. Therefore, it would be interesting to examine whether PD patients carrying mutations in these genes, as well as potential loss-of-function polymorphisms in PARPs, display less severe disease symptoms and have a higher life expectancy. Here, PRKN is linked to Parkinson disease.