The patient had no systemic anomalies, the optic nerves were normal, and the IOP was normal; additionally, the patient never developed glaucoma.[7] Berry et al demonstrated that FOXC1 and PITX2 physically interact, and this interaction may be essential for correct differentiation of neural crest cells during embryogenesis, thereby enabling normal anterior segment development.[8] This idea is a potential explanation for why mutations in either gene can produce equivalent phenotypes. The gene discussed is PITX2; the disease is glaucoma.