Current study found increased expression of TAP1 in human lung epithelial cells, THP-1 monocytes, HeLa cells, and Vero cells following virus infection, and overexpression of TAP1 enhanced virus replication such as influenza A virus, vesicular stomatitis virus, and human enterovirus 71 by inhibiting the virus-triggered activation of NF-κB signaling and the production of IFNs, IFN-stimulated genes, and proinflammatory cytokines (93). The gene discussed is IFNA1; the disease is viral infectious disease.