The main downstream role of proteins of the FANC pathway is to repair cross-linked DNA and rescue delayed/blocked replication forks while maintaining genomic stability, and the multiple clinical and cellular phenotypes that define FA may be caused by a single factor with multiple tissue, cellular, biochemical and molecular consequences: the unscheduled activation of the senescence programme as a major consequence of the DNA damage-induced ATM-p53-p21 axis. This evidence concerns the gene TP53 and Friedreich ataxia.