It is postulated that IFN-γ signaling during AD pathogenesis may promote the development of autoimmunity as IFN-γ overexpressing mice spontaneously develop autoantibodies (41, 42) and deletion of the IFN-γ receptor inhibits autoantibody production in lupus-prone mice (43). The gene discussed is IFNG; the disease is systemic lupus erythematosus.