FANCD2 and Friedreich ataxia: To directly establish that the involvement of hMOB2 in HR repair was independent of the Fanconi Anemia (FA) pathway-coordinated ICL unhooking process, we transiently co-depleted hMOB2 and FANCD2 (Supplementary Fig. S3D), a central component of the FA pathway [66], [67], and subsequently analysed sensitivity to mitomycin C. Cells with co-depletion of hMOB2 and FANCD2 exhibited potentiated cytotoxicity to mitomycin C treatment, when compared with single depletions (Supplementary Fig. S3E), suggesting a role for hMOB2 in ICL repair that is independent of the canonical FA pathway.