Despite some differences in ICL processing between yeast and human cells, most notably the absence of readily identifiable homologs of many FA factors, yeast does possess a putative ortholog (Mph1) of the protein mutated in FA complementation group M (FANCM) [16], [17], indicating that yeast could be a powerful model for understanding some aspects of the repair defect in FA. Here, FANCM is linked to Friedreich ataxia.