Given that TGF-β is a key mediator in the development and progression of IPF and the importance of interactions between TGF-β/Smad and Wnt signaling in IPF pathogenesis, this study indicated that Wnt5B engaged FZD8 receptor to activate noncanonical Wnt signaling, which sequentially exerted a regulatory role in TGF-β/Smad-induced effects on fibroblast activation [58]. Here, WNT5B is linked to idiopathic pulmonary fibrosis.