To complement structural studies, seminal aqueous humor dynamic physiological experiments were conducted by Morton Grant and others . Using a basic aqueous humor perfusion rig, outflow facility was measured in both normal and glaucomatous enucleated human eyes before and after TM removal . We have re-organized Morton Grant’s results into one table based on outflow resistance to better summarize the results. First, the TM was the primary resistor for AHO (~70–75% incorporating data from Morton Grant and others ) (Table 1; blue arrow). Second, glaucoma eyes showed more AHO resistance compared to normal eyes (Table 1; green arrow). These two observations provided the basis for conventional AHO research and clinical thought in normal and glaucomatous eyes for the next half-century. Changes to extracellular matrix , cytoskeletal changes , secreted pro-fibrotic factors , theories of funneling , and TM biomechanics  have all contributed to a model explaining impaired outflow at the level of the TM.