This conclusion is also supported by the fact the STAT3 loss-of-function (AD-HIES) and STAT1 gain-of function patients share immunological phenotypes (e.g., defective IL-17 production in CD4+ T cells and impaired production of antigen-specific antibodies) and clinical manifestations (e.g., mucocutaneous candidiasis)12,24,29,30. The gene discussed is CD4; the disease is Alzheimer disease.