Patients with autosomal dominant hyper-IgE syndrome (Job’s syndrome, caused by STAT3 mutation) have defects in IL-6, IL-23 and IL-22 signaling with reduced TH17 cells, and are prone to have mucocutaneous candidiasis, staphylococcus aureus infection, and probably viral infections (27). This evidence concerns the gene STAT3 and Autosomal dominant hyper-IgE syndrome.