Given that optimal therapy in patients with FRDA could be considered replenishment of FXN itself, e.g. via gene therapy (Perdomini et al., 2014) or improvement of Fxn transcription via small molecules (Gottesfeld et al., 2013), we asked how much of the behavioral, physiological, pathological and molecular phenotype(s) observed at this relatively severe stage of illness could be reversed following such ‘optimal’ therapy. The gene discussed is FXN; the disease is Friedreich ataxia.