Excess TH1 (IFNγ) results in secondary excess in TNF (207). TNF activates RIP1 and RIP3, induces robust reactive oxygen species, programmed necrosis (necroptosis), and TB cavitation (76, 77) (Figure 4B). IFNγ also increases CXCR3 (a receptor for several angiostatic chemokines), causing hypoxia and granuloma necrosis (211). Excess IFNγ-induced IDO-1 (259) can also inhibit iBALT formation. This evidence concerns the gene CXCR3 and tuberculosis.