IFN-γ–activated macrophages require HIF-1α to mount effective antimycobacterial responses; myeloid HIF-1α deficiency increases TB susceptibility in vivo, and IFN-γ drives a HIF-1α-dependent shift to aerobic glycolysis, which supports effector functions (Braverman et al., 2016). The gene discussed is HIF1A; the disease is tuberculosis.