The mechanism of the optic nerve damage in open angle glaucoma has challenged the ophthalmology community for more than one century. Previous theories can not fully interpret all clinical phenomenon. Based on the pathophysiology of optic nerve in open angle glaucoma and its well-established clinical manifestations, such as elevated intraocular pressure, optic disk cupping and characteristic visual field defect, I proposed a following new hypothesis on the mechanism of glaucomatous optic nerve damage. Physiologic optic disk cup which naturally formed by optic nerve fibers converging and backward bending, is the weakest site of optic nerve head, and might be gradually deepened and enlarged under long lasting insults of intraocular pressure. The enlarged optic disk cup have changed the conformation and developed three curves of optic nerve fiber. The curves occurred against the points of hard connective tissue at the lateral front edges of lamina cribrosa pores and at the optic disk edge are injurious, which might block the axonal transport, and resulted in retrograde retinal ganglion cell lose. By using this hypothesis, new explanations for the ocular hypertension, the normal tension glaucoma and the characteristic glaucomatous visual field defect have been illustrated. And also a new surgery to prevent or postpone the glaucomatous optic nerve damage by vitrectomy and implants to level up the enlarged optic disk cup has been suggested.