Transduction of FAAP100WT rescued the defect in 1176 cells (Supplemental Figure 6, A and B), whereas we observed no significant change in FANCD2 foci formation by the transduction of either type of FAAP100 in FA-B fibroblasts (deficient) or non-FA normal control fibroblasts (proficient) (Supplemental Figure 6C). The gene discussed is FAAP100; the disease is Friedreich ataxia.