The mechanistic target of rapamycin (mTOR) signaling pathway plays a crucial role in the development, maintenance, and injury response of the human optic nerve. In retinal ganglion cells (RGCs), whose axons constitute the optic nerve, mTOR regulates axonal growth, protein synthesis, and metabolic support. During development, mTOR activity is essential for axon elongation and myelination. In the adult optic nerve, however, mTOR activity is tightly regulated, and its suppression contributes to the limited regenerative capacity of RGCs after injury. Reactivation of mTOR signaling, particularly mTORC1, has been shown in experimental models to enhance axon regeneration following optic nerve crush or glaucomatous damage. However, chronic or excessive mTOR activation may lead to maladaptive effects, including increased metabolic demand, mitochondrial dysfunction, and susceptibility to degeneration. Balancing mTOR activity appears critical for promoting neuronal survival while avoiding excitotoxicity or axonal stress. Targeted modulation of mTOR may offer therapeutic potential in optic neuropathies, including glaucoma and ischemic optic neuropathy, by enhancing neuroprotection and promoting regenerative responses.