TP53 and Friedreich ataxia: BMF, MDS and AML in FA are associated with DNA damage accumulation and genetic instability but also with alterations in senescence [35, 36]; nucleolar homeostasis and ribosome biogenesis [37–39] as well as in the activity of several stress signaling pathways, such as p38MAPK, PI3K/AKT and NF-kB [40–42]; increased expression or sensitivity to several proinflammatory cytokines, such as TNFα and TGFβ [41, 43, 44]; and the unrestrained expression or activity of p53 [45, 46], Myc [47] and/or microphthalmia transcription factor (MiTF) [48].