Lastly, our findings that FcγRIIB functions independently of the BCR to eliminate PCs and inhibit naïve B cell activation while preserve the long-lived memory B cells supports its safe clinical use not only in targeting B cells for the treatment of autoimmune diseases, e.g. SLE, but also in suppressing autoantibody-mediated destruction to tissues or cells by intravenous immunoglobulin therapy (IVIg), e.g. immune thrombocytopenic purpura. This evidence concerns the gene FCGR2B and systemic lupus erythematosus.