To delve deeper into the nature of DNA lesions generated by the NIF metabolite, we utilized two clones of HeLa cells lacking either ERCC1 (ERCC1KO)42 or FANCD2 gene (FANCD2KO)43, two proteins crucial for DNA damage repair and engaged by the Fanconi anemia (FA) pathway44(Fig. 3F). The gene discussed is ERCC1; the disease is Friedreich ataxia.