FXN and Friedreich ataxia: Overall, our findings indicate that, since most FRDA patients appear to carry primarily pure GAA repeat expansions throughout most of the length of the repeat, they are likely to exhibit a classical FRDA phenotype, showing well established decreases in frataxin gene expression due to epigenetic changes, R loop and heterochromatin formation, with consequential mitochondrial dysfunction, oxidative stress, and cell death, especially of large sensory neurons (Campuzano et al., 1996; Saveliev et al., 2003; Groh et al., 2014; Abeti et al., 2015, 2016, 2018a,b).