Every year, numerous patients successfully receive corneal transplants because this tissue is both immunologically privileged and it has a remarkable resilience to injury induced neovascularisation.¹ The biological explanation of this gift to man and woman in their quest for sustaining life-long vision, enabling corneal transplantation and the more recent corrective vision surgery a reality, has thus far remained an enigma. Notwithstanding, the search for molecules that allow the cornea to preserve its avascular status has rifled through a long list of known antiangiogenic agents, but the testing of experimental mouse models of their deficiencies have all come up without suitable answers.² This negated explanation for a single gene product being responsible for corneal avascularity spawned the next logical idea that biological redundancies in antiangiogenesis could explain the mystical properties of the cornea. Now, contrary to this belief, Ambati et al, looking at eyes from a wide range of mammalian species, have concluded in a recent report that such a formidable antiangiogenic role is, after all, a …