Heterozygous loss of STAT3 can be tolerated to different extents and contributes to immunological deficiencies, most commonly autosomal-dominant Hyper IgE syndrome (AD-HIES) as a result of a reduced STAT3-mediated Th17 T-cell response [27,28,29]. Here, STAT3 is linked to Autosomal dominant hyper-IgE syndrome.