In addition to the sporadic off-target mutations induced by AID in B cells, APOBEC3A and 3B are thought to be responsible for many of the non-clustered/non-kataegic mutations at TpC dinucleotides observed not only in breast cancers but in other tumour types where the kataegic signature is not obviously present (Kuong and Loeb, 2013). Here, APOBEC3A is linked to breast carcinoma.