We hypothesize that differences in the robustness of the initial proinflammatory response between non-primed resting macrophages, which are primary sites of infection, versus macrophages located in the vicinity of infected cells or infiltrating lymphocytes, are directly correlated with the priming of neighboring macrophages and their pre-exposure to TNF-α or/and IFN-γ. The gene discussed is TNF; the disease is infection.