From the results of the Ocular Hypertension Treatment Study emerged the conclusion that ocular hypertensive subjects with thinner central corneal thickness (CCT) are at increased risk of developing glaucoma. Although possible underlying biases that could have led to this conclusion are still under investigation, there is an increasing interest in the scientific community to understand the potential mechanisms of this increased risk profile. It has been proposed that interindividual differences in CCT might be purely responsible for inaccuracies of the tonometric readings with potential underestimation of the true IOP in subjects with thinner CCT although it is becoming progressively clearer that the true IOP is unpredictable with linear correction formulas for CCT, and it is likely that other material properties of the cornea contribute, together with CCT, to the tonometric artifact. Recently, it has become possible to measure the biomechanical properties of the cornea in vivo and it has been suggested that differences in corneal biomechanics may be the expression of interindividual structural differences of the ocular tissues (including lamina cribrosa), with potential consequences on the interindividual susceptibility to the glaucomatous damage under the same IOP level. A possible underlying biological risk related to thinner CCTs, independent of the influence on tonometric reading, has been proposed and largely studied after the results of the OHTS were published. Besides the understanding of the mechanism underlying the role of CCT as a risk factor for the development of glaucoma, it is important to understand how the information about CCT should be integrated in the clinical management of both ocular hypertension (OHT) and glaucoma and whether other ocular properties should be measured to better understand the individual risk profile.