Our observation that patients with active opportunistic infections had higher levels of antibody against IFN-γ compared to cases with “inactive” opportunistic infections is consistent with the hypothesis that IFN-γ autoantibody may be the cause of immunodeficiency in patients with unusual and often disseminated infections by intracellular microorganisms [4]–[9]. The gene discussed is IFNG; the disease is Immunodeficiency.