Interestingly, mice lacking Tlr4 also spontaneously develop chronic otitis media (MacArthur et al., 2006), owing to their inability to mount a sufficient inflammatory response to bacterial pathogens; the observation of a similar phenotype in the Splunc1−/− mouse suggests that these mice suffer from a deficiency in Tlr4-mediated inflammation owing to altered responsiveness to LPS. The gene discussed is BPIFA1; the disease is chronic otitis media.