Whereas no human “knockout” equivalent has been found for AHR, CYP1A1, or CYP1A2, null mutations in CYP1B1 are associated with primary congenital glaucoma [44], suggesting that, during embryogenesis, development of the eye’s anterior chamber requires metabolism of a critical endogenous CYP1B1 substrate, most likely a lipid mediator [34]. The gene discussed is CYP1B1; the disease is primary congenital glaucoma.