Recently, Bhorade et al1 showed that there is an up-regulation of interleukin (IL)-15 protein in BAL fluid in lung transplant patients with acute rejection receiving the IL-2 blocking agent daclizumab. This is a very interesting finding; however, we can hardly agree with their results of BAL fluid cellular analysis. In fact, using 90 mL of normal saline solution, they found in the BAL cellular differentiation higher percentages of neutrophils and lymphocytes in the control patients compared to the rejectors (17% and 14%, respectively, compared to 9% and 9%). Moreover, there must be a mistake in the percentages because they add up to > 100%.1Although these results were not significantly different between groups, they are quite unusual. Indeed, several authors have shown that acute cellular rejection represents a lymphocytic perivascular infiltration with an increase in BAL lymphocytes,2which also correlates with the severity of acute rejection.3We have recently published a study4 in patients with acute lung rejection in which we corroborated these results, but we were also able to demonstrate an increased level of IL-17 protein in their BAL fluid, and this was accompanied by an increased BAL neutrophilia, which also correlated with the severity of the acute rejection. At the same time, there was an increase in IL-8 protein in the BAL fluid that correlated with the BAL neutrophilia.4As a consequence, we hypothesized that IL-17, which may stimulate airway epithelial and smooth-muscle cells to release Il-8,5 is indirectly responsible for the BAL neutrophilia during acute rejection. This is in contradiction to what the authors demonstrate in the present study.1 We would like to ask the authors how they could explain their current BAL fluid cellular differential results in view of our recent findings?