The clinical relevance of these findings is highlighted by the recent description of the role of XBP1 in the control of antitumor immunity and in the disruption of DCs homeostasis (13), as well as by sound hypotheses associating ER stress caused by HLA-B27 misfolding with IL-23 production in a rat model of spondyloarthritis (14) and the involvement of the IL-23/IL-17 axis in triggering tumor-elicited inflammation and tumor growth (15). The gene discussed is IL23A; the disease is neoplasm.