In this context, an overexpression of mature lung-specific Wnt5A was found to functionally attenuate canonical Wnt-driven alveolar epithelial cell wound healing and transdifferentiation in vitro, which in turn exacerbate airspace enlargement in elastase- or CS-induced experimental emphysema in vivo [46]. The gene discussed is WNT5A; the disease is pulmonary emphysema.