Th1 immune responses, particularly the interleukin 12 (IL-12)/gamma interferon (IFN-γ) axis, are thought to be pivotal host factors in protection against disseminated MAC disease, because patients who have insufficient immune responses involving the IL-12/IFN-γ axis or patients who have IFN-γ autoantibodies often develop disseminated and extrapulmonary MAC disease (2, –, 4). This evidence concerns the gene IFNG and Mycobacterium avium complex disease.