The role of disrupted homologous recombination (HR) in human cancer susceptibility is well established by studies of tumor incidence in BS, where loss of the BLM helicase increases inter- and intrachromosomal recombination [120] and the high incidence of breast and ovarian cancer in carriers of BRCA1 mutation, where loss of BRCA1 suppresses HR and impedes DNA double-strand break repair [139]. This evidence concerns the gene BRCA1 and neoplasm.