Maintenance of normal corneal transparency and the possible loss of it in disease continue to be relevant clinical issues. The possibility of control of corneal hydration (hence transparency) by the active intervention of the corneal limiting layers was raised for the first time by Davson in an article in the BJO in 1949.1 Thanks to the discovery of endothelial fluid transport by Maurice2 and the contributions of, among others, Mishima,3 Dikstein,4Fischbarg,5 Hodson,6 Green,7Edelhauser,8 Wiederholt,9 Riley,10Bonanno,11 and their colleagues, it is clear that the corneal endothelium dehydrates the cornea and contributes to the maintenance of its transparency.

Such understanding and the fact that endothelial cells do not divide in humans has led to substantial advances in the way the endothelial layer is treated during surgery or is preserved before transplantation. Still, endothelial loss of function or decompensation continues to be a clinical problem, which raises the question of whether what has been gained in recent basic knowledge can now be put to renewed clinical or therapeutic use. In this context, after nearly five decades since the modern chapter of endothelial function began, it seems fitting to ask once more how this layer might function.