In contrast, the MMC sensitivity of FANCA-deficient U2OS or FA-A patient cells depleted of MSH2 was not suppressed (Fig6A and B, and Supplementary Figure S8D–G), suggesting FANCA functions in ICL processing in a manner distinct from FANCJ, BRCA1, or FANCD2. The gene discussed is MSH2; the disease is Friedreich ataxia.