Wild-type BRCA1 and BRCA2 are tumour-suppressor genes and their protein products have multiple functions, including serving as key enzymes in the homologous recombination pathway, which is the high-fidelity mechanism for repair of DNA double-strand (DS) breaks.28,29 Loss-of-function mutations or silencing of BRCA1/2 disables the homologous recombination pathway, which forces cells to rely on lower fidelity more error-prone pathways for DNA repair, such as non-homologous end-joining, during which mutations and genetic instability may be introduced.30–32. This evidence concerns the gene BRCA1 and neoplasm.