In vitro studies of wound healing have demonstrated that WNT5A induces cell migration and assists in wound closure suggesting a potential role in preventing fibrosis.13, 20, 21 A few studies have revealed elevated levels of WNT5A in fibrosis of the liver 22 and in patients with idiopathic pulmonary fibrosis and acute lung injury.23, 24, 25 Although these studies shed some light on the gene expression profile of WNT5A, further investigation is required to understand why WNT5A is up‐regulated during wound healing and fibrosis and if it is exerting a positive or negative effect. This evidence concerns the gene WNT5A and idiopathic pulmonary fibrosis.