Disseminated infection with M. avium before six years of age is a hallmark of a lack of IFN-γ immunity due to inherited defects of the IFN-γ response pathway4,5,12,34, whereas M. avium disease at a later age may be due to profound deficiencies as a result of the production of anti-IFN-γ auto-antibodies92,93, or a severe progressive quantitative defect of IFN-γ myeloid target cells caused by GATA2 deficiency94,95. Here, GATA2 is linked to infection.