Pastorelli et al. [54] reported that usage of anti-TNF-α therapy (infliximab) decreased circulating IL-33 in UC patients and that level of IL-33 was significantly increased and correlated with disease severity, suggesting that the IL-33/ST2 system plays an important role in IBD pathogenesis and it is modulated by anti-TNF-α therapy and may represent a specific marker for active UC [48, 49, 54]. The gene discussed is IL33; the disease is inflammatory bowel disease.