This agent coengages BCR and FcγRIIb, making splenic and lymph node B cells hyporesponsive to BCR activation for more than two weeks in SLE‐prone B6.hRIIb and NZM.hRIIb mice, which were genetically modified to express the human FcγRIIb extracellular domain [176]. This evidence concerns the gene BCR and systemic lupus erythematosus.