Sequential infection significantly increased the concentration of proinflammatory cytokines IFN-γ, IL-6, and TNF-α, which were ≥280, 24, and 15 times higher than that seen in SPfree mice, respectively (Fig. 2B, 2C), clearly demonstrating that sequential infection with common experimental pathogens elevates the systemic inflammatory response. The gene discussed is TNF; the disease is infection.