For example, the loss of function mutations in BRCA1 and BRCA2, two genes important for the repair of double‐strand breaks (DSBs) through homologous recombination (HR), accounts for a large fraction of hereditary breast and ovarian cancers.2 On the other hand, genome instability has also been exploited for cancer therapy with the idea that additional instability brought about by chemotherapy agents or radiation would push cancer cells into death or senescence due to the accumulation of excessive DNA damages. This evidence concerns the gene BRCA2 and cancer.