They included the following components: i) Those contributing to homologous recombination (HR), such as BRCA1, RAD51D, MRE11A, and RAD51B; ii) Those involved in Fanconi anemia (FA), such as FANCG, FANCA, SLX4, BLM, FANCD2, FANCL, and BRIP1; iii) Those involved in base excision repair (BER), such as MUTYH; iv) those involved in nucleotide excision repair (NER), such as ERCC2; v) those involved in mismatch repair (MMR), such as MLH1, MSH2, MSH3, MSH6, PMS1, and EPCAM; vi) those contributing to DNA sensor (DS), such as ATM and CHEK2 (Figure 1B). This evidence concerns the gene BRIP1 and Friedreich ataxia.