IL6 and hyper-IgE syndrome: For example, the finding that mutations in STAT3 (which transduces signals from IL-6, a canonical Th17 cytokine) can lead to hyper-IgE syndrome (HIES) led to the discovery that this subset of HIES patients fail to generate Th17 cells, potentially accounting for their susceptibility to fungal infection (Ma et al., 2008).