In contrast, Tlr7−/− BMDMs secreted similar levels of tumor necrosis factor alpha (TNF-α) during infection with KIM6 or the ΔphoP mutant, suggesting that TNF-α secretion by infected macrophages occurs through a different pathway that is neither dependent on TLR7 nor significantly impacted by bacteria that lyse in the intracellular compartment (Fig. 1D). The gene discussed is TNF; the disease is infection.