The mechanistic target of rapamycin (mTOR) plays an essential role in regulating cellular proliferation, differentiation, and metabolic homeostasis within the human lens. During lens development and maintenance, mTOR activity governs epithelial cell proliferation and fiber cell elongation, processes essential for preserving lens transparency and structural integrity. Dysregulation of mTOR signaling has been associated with age-related cataractogenesis, partly through impaired autophagy, oxidative stress accumulation, and altered protein homeostasis. Inhibition of mTOR, particularly mTORC1, has been shown to enhance autophagic flux, reduce reactive oxygen species, and stabilize crystallin proteins, thereby delaying cataract formation in experimental models. Thus, mTOR represents a key molecular integrator of growth and stress responses in the lens, with potential therapeutic implications for age-related and metabolic cataracts.