Several mechanisms of action have been described for antibodies targeting flaviviral NS1, such as blocking the endothelial permeability caused by NS1 protein (15), reducing the production of progeny virions through FcγR-dependent cytolysis of the infected cells (36, 37), or suppressing viral infection through both FcγR-dependent cytolysis and an unknown FcγR-independent pathway (38, 39). The gene discussed is FCGR2A; the disease is viral infectious disease.