For instance, keratinocyte-derived IκBζ was found to drive psoriasis (50, 51); and mice deficient in IκBζ are resistant to EAE due to a defect in Th17 development, explainable by the fact that IκBζ enhances IL-17 expression by directly binding to the regulatory region of the Il-17 gene (16). The gene discussed is IL17A; the disease is psoriasis.