Nevertheless, significant chromosomal aberration in uncorrected FA-iPSCs [25], but not in FA-iPSCs derived from “corrected” somatic cells [26] or in human ESCs with stable knockdown of FANCC [25] suggests that the FA pathway is required to prevent DNA damage and chromosomal instabilities associated with the reprogramming process. The gene discussed is FANCA; the disease is Friedreich ataxia.