Notably, this cluster includes key components of the homologous recombination (HR) and Fanconi anemia (FA) repair systems—such as BRCA1, XRCC3, BRIP1, BARD1, FANCA, and FANCG—which act in concert to detect and resolve DNA double-strand breaks (DSBs) and inter-strand crosslinks (ICLs), two of the most cytotoxic forms of DNA damage [37,38]. This evidence concerns the gene FANCG and Friedreich ataxia.