A recent discovery suggests that IL-36 cytokines may serve as a novel focus for addressing IBD and atopic diseases.[38] Increased expression of IL-36α and IL-36γ was detected in colon biopsy tissues of patients with active IBD.[39,40] Additionally, IL-36R-/- mice subjected to acute dextran sodium sulfate-induced (DSS-induced) colitis exhibited up-regulation of IL-36α and IL-36γ.[41] Furthermore, IL-36R signaling enhances the Th1 response while suppressing the Th17 response. The gene discussed is IL36G; the disease is inflammatory bowel disease.