These reports indicate that epithelial cells derived IL-18 is sufficient to generate, transform and accumulate pathogenic eosinophils to esophageal epithelial mucosa. Therefore based on these novel findings, we propose several approaches to improve human EoE pathogenesis by proposing to conduct a clinical trial of IL-18 neutralization, and also inhibiting NLRP3, caspase1 using respective antagonist. This evidence concerns the gene IL18 and eosinophilic esophagitis.