Emerging functional studies in fibrosis have suggested a more deleterious role for WNT5A in fibrosis,23, 26 and most have shown WNT5A to exacerbate injury in the presence of FZD receptors.31 For instance, in a study of asthma development WNT5A and TGFB resulted in ECM production in airway smooth muscle cells and these cells demonstrated high levels of FZD8. This evidence concerns the gene TGFB1 and asthma.