CMR of C. burnetii can induce nonspecific immunoresponses, producing high levels of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) in hosts [22,23], which inhibit viral, protozoan and bacterial infections via activation of bactericidal systems of macrophages and cytotoxicity of NK cells [24]. The gene discussed is TNF; the disease is bacterial infectious disease.