Deficiencies in homologous recombination (HR), transcription‐coupled nucleotide excision repair (TC‐NER), and DNA mismatch repair (MMR), along with replication slippage, activity of the AID/APOBEC family of cytidine deaminases, and reduced RAD52 expression, are key contributors to the mutagenesis of these sites in cancer [3, 13]. This evidence concerns the gene AICDA and cancer.