Based on these studies, which all argue for a crucial role of Wnt/β-catenin signaling in the pathogenesis of glaucoma, it is tempting to speculate that a comparable scenario in DBA/2J/Pax6-Norrin mice might involve the Norrin-induced activity of canonical Wnt/β-catenin signaling attenuating the continuous structural changes in the chamber angle of DBA/2J/Pax6-Norrin mice, albeit not to an extent that significantly interferes with IOP elevation. The gene discussed is PAX6; the disease is glaucoma.