A reduced RORγt expression and the consequent impairment of Th17 cell generation (23) have been described in patients with APECED (Autoimmune PolyEndocrinopathy with Candidiasis and Ectodermal Dystrophy) due to mutations of the AIRE (AutoImmune REgulator) gene (24) and hyper-IgE recurrent infection syndromes (HIES) due to mutations of the signal transducer and activator of transcription 3 (STAT3) (25–28), tyrosine kinase 2 (TYK2) (29, 30), dedicator of cytokinesis 8 (DOCK8) (31, 32), and RORC genes (33). Here, DOCK8 is linked to hyper-IgE syndrome.