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The phenotype of human glaucoma1 spans from 'shallow' through 'deep' forms of 'cupping'. 'Senile sclerotic'2 cupping classically occurs in elderly eyes that demonstrate 'shallow' enlargement of the cup, pale rims and peripapillary atrophy. What determines, and can we predict, the eye-specific phenotype an ocular hypertensive eye will manifest as it becomes detectably 'glaucomatous'? In this report Jung et al., add to two previous retrospective analyses,3,4 (one their own),3 and a third that was prospective,5 which find age to be inversely related to SDOCT-determined laminar depth in glaucoma subjects within an analysis that controls for IOP and severity of damage (visual field MD and or retinal nerve fiber thickness). A similar relationship was present in their previous study3 of a small group of primary open angle glaucoma patients (but not within a larger group of normal tension glaucoma subjects). Ren et al.4 found age to inversely correlate to laminar depth within high risk ocular hypertensive and early glaucoma subjects. Unlike the present report, neither of the prior studies found strong relationships to initial or treated IOP. These data suggest that ONH 'aging' increases ONH structural stiffness and also that structurally stiff eyes of all ages will deform less for a given level of IOP insult. These findings are important because they contribute to a scientific explanation of phenotype that will allow us to predict the appearance a given eye will demonstrate at a given level of IOP. Study limitations (as in all like it) include the fact that neither the actual IOP nor the actual age at the time of IOP elevation (and/or initial laminar deformation), can be known. Nor has this (or any) study, determined ONH structural stiffness at the start of the study and then longitudinally assessed laminar deformation while controlling for the level of IOP at which the deformation occurs.