The role of neutrophil as sentinels of the gut mucosa is well-recognized,16 and defects in neutrophil function alter the inflammatory state and microflora in the gut.18 There is compelling evidence that MPO−/− mice exhibit aberrant immune responses beyond those directly due to neutrophil activity, including both exaggerated as well as muted inflammatory responses.35–37 When studied in experimental models of colitis, MPO−/− mice show less inflammation and more rapid resolution38 or no protection33 in comparison to the responses of WT mice. The gene discussed is MPO; the disease is colitis.