We showed that psoriasis patients with a particular variant (GG) of the anti-inflammatory TNF-α-induced protein 3 (TNFAIP3) gene (BJD 2016) did not respond well to an inhibitor of IL-17, a pro-inflammatory cytokine. Remarkably, this gene was also involved in the response of IBD patients to inhibitors to another pro-inflammatory cytokine, TNFa. We found that anti-TNFa treatment of IBD patients can lead to IL-17 production through inhibition of TNFAIP3 (JACI 2017, and comment). This puts TNFAIP3, combined with IL-17A expression, on the map as a potential tool for predicting therapy responsiveness or side effects of anti-TNF or anti-IL-17 therapy. Moreover, it provides novel targets related to TNFAIP3 activity for improved therapeutic regimens in patients with inflammatory disease.