Most importantly, we demonstrated that AMBRA1 restores mitophagy in mouse embryonic fibroblasts from PINK1−/− mice, but also in fibroblasts from PD patients, in which PINK1 and PARKIN were mutated; altogether, these findings highlighted AMBRA1 as an alternative mediator of mitophagy to maintain mitochondrial homeostasis in PINK1-PARKIN-related PD (Strappazzon et al., 2015). This evidence concerns the gene AMBRA1 and Parkinson disease.