In contrast, the KIKI and KIKO models, which exhibit GAA-repeat-induced frataxin deficiency but only a mild FRDA-like phenotype, have been more useful to investigate epigenetic-based frataxin-increasing drug therapies, such as histone deacetylase (HDAC) inhibitors (Rai et al., 2010; Rai et al., 2008). The gene discussed is FXN; the disease is Friedreich ataxia.