WNT3A and idiopathic pulmonary fibrosis: A significantly downregulated ICAT, but upregulated Wnt3A, β-catenin, Wnt5A/B, DAAM1, and NLK, was observed in normal-looking parenchyma of IPF lungs as compared with healthy lungs, suggesting an association of the degree of fibrosis and the interaction between β-catenin and Wnt5A/B in IPF [9].