Due to the random nature of V(D)J recombination, the primary antibody repertoire of naïve B cells is of low affinity. In order to increase the affinity and change the effector function of antibodies, activated B cells undergo further genetic alterations of the Immunoglobulin (Ig) locus in the form of somatic hypermutation (SHM) and class switch recombination (CSR), followed by cellular selection. Said processes are collectively known as secondary antibody diversification and are essential for an effective adaptive response. SHM is characterized by mutations in the variable (V) exon at the rate of ~10-3 muts/bp/generation, approximately a million fold higher than the background genome mutation rate. CSR involves double strand breaks (DSB) in switch (S) sequences upstream of constant (C) exons. Both processes are initiated by the DNA-mutating enzyme activation-induced cytidine deaminase (AID). Although AID is essential for a proper antibody response, it is now irrefutable that AID activity results in many aggressive types of leukemia/lymphoma such as Burkitt’s lymphoma (BL), diffuse large B cell lymphoma (DLCL), follicular lymphoma (FL), multiple-myeloma (MM) and chronic lymphocytic leukemia (CLL), by mutating and/or causing chromosomal breaks in many other genes in the B cell genome. Thus, AID is the most dangerous mutator of the human genome. The purpose of our work is to characterize the molecular mechanisms of AID. Here we present our work characterizing mutants and species-variants of AID, providing insight into the mechanisms of AID action and its role in the balance between immunity and cancer.