TP53 and Friedreich ataxia: Indeed, it has been proposed that BMF in FA relies on HSC attrition resulting from a combination of alterations in cell proliferation associated with unscheduled p53 [45, 47], MiTF [48] and/or MYC [47] expression and increased accumulation of DNA damage and genetic instability that arises when HSCs exit quiescence [62, 63], which pushes cells through differentiation, limiting self-renewal of potentially mutated HSCs [64, 65].