The persistent neutrophil influx into the lungs of TLR2−/− mice may result from the inability of neutrophils to undergo apoptosis, however, we show that TLR2−/− neutrophils have reduced phagocytic capacity (Figure 7), and this may be the mechanism that leads to persistent infection (possibly including within the compromised neutrophils) and excessive and prolonged neutrophil recruitment. The gene discussed is TLR2; the disease is infection.