The significance of nuclear IL-33 sequestration and the great potency of IL-33/ST2 signaling in developing acute inflammation was presented by Carriere et al. The results of this study demonstrated that an alteration in the N-terminal part of IL-33 impeded the interaction of the cytokine with chromatin, resulting in the development of an inflammatory response, with splenomegaly, elevated lymph node influx, and colitis development [34]. This evidence concerns the gene IL1RL1 and colitis.