Given the results detailed above, particularly the potent enzymatic activity of A3H-I with an intrinsic preference for cytosines in a TC context, the capacity of A3H-I to mutate a variety of substrates, and the ability of A3H-I to breach the nuclear compartment, we next performed a comprehensive analysis of all available TCGA tumour data sets with n-values >400 exomes to begin to assess whether A3H-I is a general source of mutation in cancer or a unique mechanism that compensates for the loss of A3B in a limited subset of breast cancers. Here, APOBEC3B is linked to breast carcinoma.