Further, all the REP mutations were able to restore a phospho-dead PRKN variant (PRKNS65A) [29] and PRKNW403A was earlier shown to rescue the mitophagy activity of several PD-associated PRKN mutations when overexpressed in cis with the aforementioned mutations in U2OS cells [18,30]. This evidence concerns the gene PRKN and Parkinson disease.