Tulek et al. [35] demonstrated that, in pulmonary fibrosis, the antifibrotic effect of Rapamycin can be explained by an anti-inflammatory effect mediated by a decrease in IL-13 and platelet-derived growth factor- (PDGF-) A and TGF-β1 and an increase in interferon- (IFN-) γ levels in bronchoalveolar lavage fluid. The gene discussed is IL13; the disease is pulmonary fibrosis.