Somatic hypermutation at antibody loci affects both deoxyadenosine-deoxythymidine (A/T) and deoxycytidine-deoxyguanosine (C/G) pairs. Deamination of C to deoxyuridine (U) by activation-induced deaminase (AID) explains how mutation at C/G pairs is potentiated. Mutation at A/T pairs is triggered during the initial stages of repair of AID-generated U lesions and occurs through an as yet unknown mechanism in which polymerase η has a major role. Recent evidence confirms that human polymerase η can act as a reverse transcriptase. Here, we compare the popular suggestion of mutation at A/T pairs through nucleotide mispairing (owing to polymerase error) during short-patch repair synthesis with the alternative proposal of mutation at A/T pairs through RNA editing and RNA-directed DNA repair.