[5] It creates mutations in DNA[6][7] by deamination of cytosine base, which turns it into uracil (which is recognized as a thymine).

The cell's DNA replication machinery recognizes the U as a T, and hence C:G is converted to a T:A base pair.

[11][12][13] The involvement of Cis-regulatory factors is suspected as AID activity is several orders of magnitude higher in the immunoglobulin "variable" region than other regions of the genome that are known to be subject to AID activity.

[17] At the post-transcriptional level of regulation, AID expression is silenced by mir-155, a small non-coding microRNA[18][19] controlled by IL-10 cytokine B cell signalling.

[21] In certain haematological malignancies such as follicular lymphoma persistent AID expression has been linked to lymphomagenesis.