Alexandrov et al. [15] mapped the overall mutational catalogues for each individual cancer genome and assigned signatures due to (1) exogenous agents, for example, tobacco smoking or ultraviolet (UV) light; (2) endogenous sources, including replication and repair of DNA double-strand breaks (DSBs) through non-homologous end-joining – an error-prone pathway that re-ligates broken ends of DNA without filling in the gaps causing loss of genetic information; and (3) defective DNA repair mechanisms, such congenital as mutations in BRCA1 or BRCA2 that increase base substitutions and deletions [17]. The gene discussed is BRCA2; the disease is cancer.