The administration of SLE- or T1DM-chimeric molecules resulted in a significant reduction in anti-dsDNA or anti-GAD65 IgG antibody-producing plasma cells, inhibition of disease-associated cell proliferation, induction of B- and T-lymphocyte apoptosis as well as reduction in proteinuria and glomerular deposition of human IgG immune complexes in humanized immunodeficient SCID mice reconstituted with PBMCs from SLE patients [16,17,18]. The gene discussed is GAD2; the disease is type 1 diabetes mellitus.