Cells derived from patients with an inherited disease (e.g., Fanconi anemia [FA], ataxia-telangiectasia-like disorder [ATLD], Nijmegen breakage syndrome [NBS] and ligase IV syndrome) involving a defect in DNA repair proteins (FA proteins, ataxia-telangiectasia-mutated [ATM], NBS1 and ligase IV, respectively) show low reprogramming efficiency [14–19], indicating that the DNA repair pathway is also involved in reprogramming. The gene discussed is ATM; the disease is Friedreich ataxia.