TP53 and Friedreich ataxia: BM failure in FA has been proposed to be the consequence of damage accumulation in the DNA of hematopoietic stem and progenitor cells (HSPCs) and hyperactivation of growth suppressing pathways, such as the TGFβ (Transforming growth factor β) and the p53/p21 pathways, thus resulting in critical reductions in the number of HSPCs [16,17].