Our group investigates the molecular mechanisms of somatic hypermutation (SHM), whereby B lymphocytes diversify the immunoglobulin genes to produce high-affinity antibodies of varying isotypes against pathogen and vaccine antigens. SHM is initiated by the mutator enzyme, activation-induced deaminase (AID), whose activity is also essential for generating antibody isotypes via class switch recombination. However, SHM is a double-edged sword because it can generate self-reactive antibodies that trigger autoimmune disease and mutate major proto-oncogenes triggering B lymphomagenesis. A deeper understanding of SHM may lead to the identification of vulnerabilities that could be targeted for the treatment of these diseases.