In addition, the crosstalk between activating FcγR (non-FcγRIIb) and the innate immune receptors (such as TLR-4 and Dectin-1) amplifies pro-inflammatory cytokine productions contribute to enhancing adaptive immunity associated with autoimmune disease by excessive inflammation [32], in FcγRIIb−/− mice also promotes the pro-inflammatory responses in active lupus with endotoxemia and glucanemia from the leaky gut [33]. This evidence concerns the gene CLEC7A and autoimmune disease.