Given that our evidence also demonstrates that Foxc2 can functionally substitute for Foxc1 during ocular morphogenesis, including the SC vasculature (Fig 8), this work may also offer insight into pathological signaling mechanisms associated with Foxc1 mutations in Axenfeld-Rieger syndrome and the progression of secondary glaucoma to identify novel therapeutic targets. The gene discussed is FOXC2; the disease is Axenfeld-Rieger syndrome.