In particular, it has been demonstrated that ectopic expression of TRAP1 is able to counteract dysfunctional phenotypes in PD models, such as those induced by α-synuclein overexpression, preventing, or attenuating, mitochondrial defects and apoptosis (Butler et al., 2012; Fitzgerald et al., 2017; Hoter et al., 2018). This evidence concerns the gene TRAP1 and Parkinson disease.