Here, we explore whether myeloablative allogeneic BMT of cells expressing the wild‐type Fxn gene can be harnessed as a potential neuroreparative gene therapy for FA; and secondly, to extend our previous studies, whether subsequent administration of G‐CSF and SCF can enhance BM‐derived cell integration within the diseased nervous system and improve therapeutic efficacy. This evidence concerns the gene FXN and Friedreich ataxia.