Furthermore, since both CS exposure and A(H7N9) virus infection trigger the release of proinflammatory cytokines and chemokines such as TNF-α4,19–22,37, the attenuated pathogenicity of A(H7N9) virus infection in the CS-exposed mice might involve inflammatory signaling, especially through TNF-α-related pathways. The gene discussed is TNF; the disease is viral infectious disease.