As anticipated, most of the DE genes leading the enrichment in HCT-15 belonged to NER (e.g. GTF2H3 and RBX1) and other recombinational pathways such as homologous repair (HR) (e.g. MMS22L and BARD1) and fanconi anemia (FA) (e.g. BRIP1 and FANCM), all better suited for the efficient repair of bulky lesions and highly toxic DSBs and crosslinks (Cantor et al., 2001; Li and Jin, 2012; Niraj et al., 2019; Piwko et al., 2016; Satoh and Hanawalt, 1996; Westermark et al., 2003). This evidence concerns the gene FANCM and Friedreich ataxia.