The development of colitis in the Gαi2−/− mouse model is dependent on the presence of an enteric microflora (unpublished observations) and is characterized by a Th1 CD4+ T cell response, with increased production of IFN-γ, together with increased levels of IL-1, IL-6 and TNF-α in inflamed tissue [1], [2], [4]. This evidence concerns the gene CD4 and colitis.