The mechanism of the reduction in airway VEGF levels in asthma induced by pranlukast administration is unclear. One report2has indicated that asthmatic patients exhibited a greater expression of VEGF receptors (flt-1 and flk-1) in the airway mucosa. Moreover, increased VEGF expression in asthmatic patients were identified by infiltrating inflammatory cells in the submucosa in order of abundance as CD34+ cells → eosinophils → macrophages → T cells → mast cells. Therefore, one possible explanation is that pranlukast administration decreased airway VEGF levels via the reduction of infiltrating inflammatory cells. We also think that analysis of cell-associated VEGF isoform (VEGF189 and VEGF206) expression is important to understand VEGF bioactivity in asthma. Though the results were not shown in our study, we examined cell-associated VEGF isoform expression by immunohistochemical analysis. On the basis of these results, we found a significant correlation between the expression of free VEGF and that of cell-associated VEGF. In our recent study,3 we determined that the interaction between airway microcirculation and VEGF may be a key element in the pathophysiology of asthma. Therefore, pranlukast administration might decrease airway microvascular permeability through, at least in part, a decrease in airway VEGF levels in asthmatic patients.