It has been found that overexpression of the high-affinity antagonist IL-13Rα2, which is related to IL-13Rα1 and can bind IL-13 but lacks any signaling capability, inhibits the fibrotic markers induced by IL-13 in vitro and in bleomycin-induced pulmonary fibrosis, indicating that IL-13Rα2 has antifibrotic properties [15]. The gene discussed is IL13RA2; the disease is pulmonary fibrosis.