Studies using cytokine‐depletion/over‐expression mice showed that lung fibrosis is strongly associated with the development of a type 2 cytokine immunity, including IL‐4, IL‐5, and IL‐13,7, 8, 9 indicating a skew in favor of type 2 cytokine milieu may be the key molecular event mediating abnormal epithelial–mesenchymal crosstalk. The gene discussed is IL13; the disease is pulmonary fibrosis.