Furthermore, they invite speculation that raising MFN1 levels could be a therapeutic strategy, possibly beyond the treatment of CMT2A, i.e., for other CMT and neurodegenerative diseases in which mitochondrial dynamics might play a role, including amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), Parkinson's disease (PD) and Alzheimer's disease (AD) (Burté et al., 2015; Wang et al., 2018a). This evidence concerns the gene MFN1 and Parkinson disease.