In addition, we found that most of the cytokines we detected, such as INF-γ, IL-1β, and TNF-α, were present at significantly higher levels in lung homogenates of Ncoa4–/– mice compared with those of Ncoa4+/+ mice at 4 weeks after infection, suggesting that NCOA4 suppresses pulmonary inflammation and impairs bacterial control. The gene discussed is TNF; the disease is infection.