Eosinophils and mast cells contain leukotrienes in abundance. Cysteinyl leukotrienes are inflammatory mediators derived from arachidonic acid. They are important in eosinophil attraction and migration, smooth muscle bronchoconstriction, vascular permeability, and mucus hypersecretion (13). Montelukast is a leukotriene receptor antagonist and blocks specifically the leukotriene D4 (LTD4) receptor. Attwood et al treated 8 patients with EE with Montelukast for which 6 reported complete subjective improvement and 5 remained asymptomatic on a maintenance regimen. Treatment with Montelukast did not change the density of eosinophils present in the esophagus however (14). Montelukast has been used in mouse models to decrease fibrosis occurring in both the liver and the lung. El-Swefy and Hassanen performed a randomized study in which they subjected mice to one of 4 groups, no bile duct ligation plus saline, no bile duct ligation plus montelukast, bile duct ligation plus montelukast and bile duct ligation plus saline. Bile duct ligation induced inflammation leading to cirrhosis and fibrosis. They found that bile duct ligation increased the amount of TGF-β, which correlated with the amount of fibrosis found. Of more import is that montelukast significantly reduced the amount of fibrosis as well as decreased the amount of TGF-β (15). Izumo, Kondo, and Nagai evaluated the use of montelukast in the prevention of pulmonary fibrosis after exposure to bleomycin. They found that mice given montelukast had significantly lower levels of TGF-β and fibrosis of the lung (16).