The mechanistic target of rapamycin (mTOR) pathway plays a critical role in regulating cellular metabolism, growth, and survival within the anterior segment of the human eye, particularly in structures involved in aqueous humor dynamics. In the trabecular meshwork and Schlemm’s canal, mTOR influences extracellular matrix remodeling, cytoskeletal organization, and cellular contractility—factors that are essential for maintaining aqueous outflow and intraocular pressure (IOP) homeostasis. Dysregulation of mTOR signaling in these angle structures has been implicated in increased outflow resistance and the pathogenesis of primary open-angle glaucoma. Enhanced mTOR activity may contribute to trabecular meshwork fibrosis, oxidative stress, and reduced autophagy, all of which impair drainage function. Pharmacological inhibition of mTOR, particularly mTORC1, has demonstrated potential to restore trabecular outflow and reduce IOP by promoting autophagic clearance and cytoskeletal stability. While mTOR also plays roles in the cornea, lens, and conjunctiva, its dysregulation in the angle is of particular relevance to glaucomatous disease, making it a promising therapeutic target for early intervention and progression control.