In this study, we found that the levels of MCP-1, TNF-α, IL-1β, PGE2, PLA2, and LTB4 in the supernatant of alveolar macrophages infected with influenza virus were significantly enhanced, while MSTL significantly inhibited the levels of those proinflammatory cytokines and mediators after virus infection in vitro. The gene discussed is TNF; the disease is viral infectious disease.