The role of TLR2 in lung inflammation later in the course of pneumonia could have been obscured by the growing bacterial load in TLR2 KO mice (that is, at 48 and 72 h after infection, TLR2 deficiency could be compensated for by the higher bacterial load, providing a more potent proinflammatory stimulus via TLR2-independent pathways). The gene discussed is TLR2; the disease is susceptibility to pneumonia measurement.