(154) found a dual opposing roles for HIF-1α in mice: (i) a protective role in early stage TB (≤28 days after infection) through macrophage activation in conjunction with IFNγ and (ii) a detrimental role at a later stage of infection through HIF-1α inhibition of apoptosis of foamy macrophages, impairing an effector mechanism by which intracellular Mtb are killed. Here, HIF1A is linked to tuberculosis.