Although the FcgRIIb defect is only a part of the genetic abnormalities in lupus, FcgR-TLR-4 cross-talk might be responsible for the hyper-immune responses against several conditions in patients with lupus through macrophages and neutrophils, and the blockage of spleen-tyrosine-kinase (Syk, a shared downstream signaling molecule of both FcgR and TLR-4) attenuates lupus-induced inflammation both in mice and in patients [31,95]. Here, FCGR2B is linked to systemic lupus erythematosus.