H7N9-infected BALB/c mice produced higher levels of proinflammatory cytokines and chemokines, including IP-10, TNF-α, MCP-1, MCP-3, IFN-α, MIP-1β, KC, and regulated upon activation normal T cell expressed and secreted (RANTES), at an early stage of infection (day 3 post-infection) than BALB/c mice infected with the H9N2 virus, but lower levels than those produced when BALB/c mice were infected with H5N1 [8]. The gene discussed is CCL4; the disease is infection.