A reduction in protein synthesis, which is one of the consequences of mtUPR activation, rescues many of the defects in flies lacking PINK1 (Liu and Lu, 2010), while Drosophila flies overexpressing a mutant OTC (ornithine transcarbamylase) protein prone to aggregation develop mitochondrial dysfunction phenotypes similar to PINK1 and Parkin mutants (Pimenta de Castro et al., 2012), further confirming the pathogenic role of protein misfolding in PD. This evidence concerns the gene PINK1 and Parkinson disease.