Of these, the recruitment of XPF/ERCC1 appears to be the most important, as knockdown of XPF (FANCQ) induces a severe FA phenotype, and a minimal SLX4 peptide which interacts only with XPF/ERCC1 has been shown to be sufficient to restore ICL repair, with SLX4 enhancing the nuclease activity of XPF/ERCC1 100-fold by directing specificity to damage sites [28]. Here, ERCC1 is linked to Friedreich ataxia.