The issue is a critical one given that mutations in the Chl1 human homologs ChlR1/DDX11 and BACH1/BRIP1/FANCJ collectively result in Warsaw Breakage Syndrome, Fanconi anemia, cell aneuploidy and breast and ovarian cancers [27], [31], [32], [34–40]. The gene discussed is BACH1; the disease is Warsaw breakage syndrome.