Patients with EE have an abundance of inappropriate cells within the esophagus, including eosinophils and mast cells. A normal esophagus is devoid of eosinophils. Mast cells likely have an active role in the development of eosinophilic esophagitis; unfortunately the precise mechanism is unknown. Mast cells are found in the majority of vascularized tissues and are abundant in the gastrointestinal tract. They are located in the submucosa and lamina propria. Within the esophagus specifically, they are found in the mucosa and submucosa with rare expansion into muscularis layer. With severe eosinophilic inflammation, mast cells can be seen in the muscularis layer. Biopsies from patients with EE have demonstrated marked increase in mast cells in the mucosal layer of the esophagus. There has been correlation of mast cell number with degree of eosinophilia. Mast cells within the GI tract contain tryptase as well as other preformed mediators and can synthesize mediators that promote inflammation. Tryptase may activate eosinophils and therefore induce eosinophilic degranulation and cytokine secretion. Mast cells release chemokines and leukotrienes specific to eosinophil recruitment. Ultimately mast cell mediators worsen edema, create more inflammation, induce smooth muscle contractility and potentially affect tissue fibrosis. Therefore, active mast cells are proinflammatory, modify esophageal function, and encourage the development of strictures (12). Mast cells may be a key component in the propagation of the inflammatory state as well as of significant importance in the development of fibrosis. Evaluating tryptase levels could lead to a better understanding of the inflammatory process and ultimate problem of fibrosis.