A paper published online today in Nature Genetics reports that the DNA-specific cytidine deaminase APOBEC3A (or A3A) is likely to be the major driver of APOBEC-mediated mutagenesis in human cancer. This finding is somewhat surprising because another deaminase, APOBECA3B (or A3B), has been considered the more likely mutator based on previous studies. Gene expression levels of APOBEC3B as well as mutagenic signatures in certain cancer types, such as breast cancer, have been consistent with a primary role for A3B in cancer-related mutagenesis. However, results of a recent paper by Serena Nik-Zainal et al. called this into question by showing that breast cancer samples from individuals with germline APOBEC3B deletions showed high levels of mutations consistent with APOBEC-dependent mutagensis.