However, A3A is a more potent DNA deaminase than A3B, and the derivation of separate A3A and A3B mutational signatures—in which A3A has been demonstrated to preferentially target YTCN sites (where Y = pyrimidine), whereas A3B preferentially targets RTCN sites (where R = purine)—suggest A3A accounts for a significantly higher proportion of the somatic mutations seen in HPV-associated cancers than A3B [61,62]. This evidence concerns the gene APOBEC3A and cancer.