Previously, studies demonstrated that aforementioned bFGF-induced α-SMA and fibronectin could be abrogated by siRNA to β-catenin, Wnt5A, or RhoA transduced by adenoviral vectors in primary fibroblasts of rats, indicating a pivotal role of the β-catenin-dependent canonical Wnt pathway and Wnt5A-mediated noncanonical Wnt signaling in mediating fibroblast morphology and function in pathogenesis of COPD [88]. The gene discussed is FGF2; the disease is chronic obstructive pulmonary disease.