Their major role in the maintenance of immunological self-tolerance and immune homeostasis (4, 5) is illustrated by the rapid development of autoimmune diseases (AIDs) in normal mice upon their depletion (4) and also by the occurrence of severe AID, allergy, and immunopathology in humans with a mutated FOXP3 gene (6). The gene discussed is FOXP3; the disease is autoimmune disease.