FXN and Friedreich ataxia: The improved understanding of the FRDA molecular pathogenesis4, 5, 7, 8, 9, 10, 43 and the TALE technology development22, 23, 24, 25, 27, 28 have both contributed to the development of our proposed therapeutic approach, which aims to activate the transcription initiation of the FXN gene to restore the normal mitochondrial function in FRDA cells.