Notably, the repair defect of smc5 DT40 cells toward cisplatin was genetically epistatic with mutations in the Fanconi anemia (FA) components, FANCC and FANCM, and with mutations in the FA‐like pathway defined by the DNA damage checkpoint clamp loader, RAD17, and the DDX11 helicase 19, 20. The gene discussed is SMC5; the disease is Friedreich ataxia.