Concurrent activation of homologous recombination (RAD51, RAD51B/C, RAD54L, NBN), the Fanconi pathway (FANCA, FANCL), and mismatch repair (MSH2, MSH6) suggests robust DNA repair circuits, which melanoma may exploit to maintain basal genomic stability during metastasis [59,63]. This evidence concerns the gene FANCL and melanoma.