Protective immunity to Mycobacterium tuberculosis infection, both in humans and experimental animals, is regulated by T cells, macrophages and cytokines, which include interferon-γ (IFN-γ), interleukin-12 (IL-12) and tumour necrosis factor (TNF).1,2; IFN-γ derived from T and natural killer (NK) cells has been shown to be essential, as mice with a disruption of the IFN-γ system are unable to restrict the growth of M. tuberculosis and succumb to the infection.3–6. The gene discussed is TNF; the disease is infection.