Understanding the host–pathogen interaction during latency and defining the conditions leading to M. tuberculosis reactivation has been the subject of numerous studies in various animal species and humans.48, 49, 50 The importance of CD4+ T cells, TNFα, interferon-γ and IL-12p40, together with the IL-1/IL-1R1 pathway, nitric oxide, reactive oxygen and reactive nitrogen intermediates, in host resistance to intracellular M. tuberculosis infection is evident from animal models and human inherited and acquired immunodeficiencies.50, 51. The gene discussed is IL1B; the disease is Immunodeficiency.