Importantly, this linkage analysis shows that the A3H gene is unlinked to A3A (or the A3A-B chimeric gene resulting from the A3B deletion), suggesting that the significant association with A3H-I and APOBEC signature mutations in A3B-null tumours may be due directly to A3H-I enzymatic activity and not to A3A (as favoured by recent studies7, 16, 17, 18, 19, 20, 21) nor to any other TC-preferring enzyme encoded by the locus. Here, APOBEC3B is linked to neoplasm.