In an extension of our previous findings (Chen et al., 2015), FA fibroblasts from FANCD2-deficient patient cells (PD20) showed defective fork restart that could be corrected by FANCD2 WT complementation, but not its monoubiquitination-defective mutant K561R (Garcia-Higuera et al., 2001) (Figure 2A). This evidence concerns the gene FANCD2 and Friedreich ataxia.