Despite the known pro-fibrotic actions of the IL-4/IL-13 axis, a recent study suggested a potential protective role for the IL-13Rα1 in a murine model of BLM-induced fibrosis; here, the authors speculated that IL-4 and/or IL-13 may act through the type 2 IL-4 receptor to regulate epithelial cell healing and immune responses to lung damage and further protection against pulmonary fibrosis (179). This evidence concerns the gene IL4 and pulmonary fibrosis.