Previously we reported that cells deleted for FancB exon 2 (fancbΔex2) exhibited a typical FA phenotype that included reduced cellular proliferation, increased MMC sensitivity, increased spontaneous and MMC-induced chromosomal abnormalities, reduced MMC-induced RAD51 foci and absent MMC-induced FANCD2 foci (38). The gene discussed is FANCD2; the disease is Friedreich ataxia.