Together, in addition to the role of polymorphisms in FcγRIIB, these studies suggest that polymorphisms in activating low affinity FcγRs may also contribute to SLE susceptibility, potentially via a shift in affinity for different IgG isotypes and which may consequently entail different immunological responses to ICs, (e.g., in lupus nephritis). The gene discussed is FCGR2B; the disease is systemic lupus erythematosus.