In 2010, we showed that many non‐lymphoid cancers display the same strand‐biased spectrum of point mutations at G:C and A:T base pairs in non‐Ig genes as observed in normal physiological Ig somatic hypermutation (SHM) of B cells, indicative of AID and ADAR1 action during transcription.14, 15 Later, we demonstrated the existence of motifs known to be associated with both AID/APOBECs and ADAR deaminases in non‐Ig genes of uninfected somatic cells.10 Also in 2013, Burns et al16 showed that APOBEC3B enzymatic action may serve as a source of mutations in breast cancer. The gene discussed is AICDA; the disease is lymphoma.