In apparent agreement with a relatively minor role for IFN-γ production in experimental colitis is the observation that IFN-γ action in general requires other Th1 cytokines, for instance even for canonical antiviral responses [28] IFN-γ as such is not sufficient and requires other Th1 cytokines as well, hence, although IFN-γ is a valuable marker for immune system polarization, its production is not sufficient for provoking such immune system proliferation. The gene discussed is IFNG; the disease is colitis.