Similarly, recombination repair gene defects can increase the rate of chromosomal aberrations and predispose to breast and ovarian cancers.[7] Conversely, active endogenous sources of mutation are agents that directly damage DNA. Some of these sources are well known, such as oxidation of guanine and hydrolytic deamination of cytosine, but many others are poorly defined.[3, 8] However, much headway has been made recently in understanding additional endogenous sources of DNA damage, with our group [9‑12] and others [2, 3, 13, 14] im‑plicating APOBEC3B, a member of the APOBEC family of single‑stranded DNA (ssDNA) polynucleotide cytosine deaminases, in cancer genome mutagenesis [Figure 1].