With respect to silicosis, both β-catenin-mediated canonical signaling and β-catenin-independent noncanonical signaling were altered in human airway epithelial cells upon silica stimulation; the Wnt inhibitor SFRP1 and noncanonical ligand Wnt5a were downregulated, while another Wnt inhibitor DKK1 was upregulated [13], despite the fact that the canonical Wnt/β-catenin signaling was reactivated in silicosis lungs [14, 15]. The gene discussed is WNT5A; the disease is silicosis.