FCGR2B and serum lipopolysaccharide activity: Here, we demonstrate another possible mechanism of active SLE that might be suitable for the use of fostamatinib represented by FcγRIIb deficient-induced excessive inflammation, partly through p38MAPK in the innate immune cell (macrophages and neutrophils), due to the prominent Syk activation in FcγRIIb−/− mice with endotoxemia and glucanemia.