Another supporting clue that excess IFNγ (and its downstream effects) may contribute to a detrimental immune response to the host is based on a study showing that IFNγ production by TH1 cells is far more important for TB control in the spleen than in the lungs and that increasing the IFNγ-producing capacity by the TH1 cells actually exacerbated the lung infection and led to more rapid mortality (77). Here, IFNG is linked to tuberculosis.