FcγRIIB−/− mice originally generated on 129 background and then backcrossed for many generations to B6 develop SLE-like disease (39–41) mediated by FcγRIIB deficiency and a remaining 0.8% genome derived from 129 including SLE-associated SLAM family genes (41). This evidence concerns the gene FCGR2B and systemic lupus erythematosus.