p53 knockdown (which per se leads to increased genomic instability and DNA damage [95]) rescues the hematopoietic defects in Fancd2−/− or Fanca−/− murine bone marrow [96, 97], suggesting that BMF in FA is due more to aberrant DNA damage signalling conveying growth-inhibitory directives than to DNA damage per se. The gene discussed is TP53; the disease is Friedreich ataxia.