The activation of transcription factors associated with TH2 differentiation (e.g. GATA3, STAT6, and c-MAF), represses TH1 or TH17 differentiation, thus inhibiting the production of type 1 and type 17 effector cytokines (e.g. IFNγ, IL-1β, TNFα, and IL-17), which are known to drive IBD pathogenicity [15–17]. The gene discussed is IL17A; the disease is inflammatory bowel disease.