TLR-2 and -4 mediate the release of cytokines TNFα, IL-6, IL-1β, IL-12 by macrophages in response to M. tuberculosis infection, which is critical for host resistance to infection due to their ability to activate cathelicidin (hCAP) and defensin mediated direct antimicrobial mechanisms 8–12 However, despite strong anti-M. tuberculosis innate immune mechanisms a substantial proportion of individuals infected with M. tuberculosis are unable to control the infection. The gene discussed is IL1B; the disease is infection.