Interestingly, a rare and novel chromosomal duplication of the entire IL-33 gene resulted in clinical features of EoE [49], whereas mouse models showed that the IL-33–ST2 axis is necessary to induce EoE [50] and to ensure homeostasis and the survival of eosinophils, as evidenced by reduced numbers of eosinophils in peripheral blood in IL-33- and ST2-deficient mice [51]. Here, IL33 is linked to eosinophilic esophagitis.