A major obstacle to functional recovery after central nervous system (CNS) injury is the failure of axons to regenerate. This is due to both an inhibitory extrinsic environment and a diminished intrinsic regenerative capacity of mature CNS neurons. Removing extracellular inhibitory molecules only allows limited axon regeneration. This study shows that modulating the PTEN/mTOR pathway can promote axon regeneration in adult retinal ganglion cells (RGCs) after optic nerve injury. Deletion of PTEN, a negative regulator of the mTOR pathway, in adult RGCs promotes robust axon regeneration. This is because mTOR activity is suppressed in axotomized RGCs, impairing new protein synthesis and contributing to regeneration failure. Reactivating the mTOR pathway by conditional knockout of tuberous sclerosis complex 1 (TSC1) also leads to axon regeneration. These results suggest that manipulating intrinsic growth control pathways can promote axon regeneration after CNS injury. PTEN deletion activates the PI3K/mTOR pathway, which controls cell growth and size by regulating cap-dependent protein translation. This pathway is suppressed in axotomized adult neurons, limiting new protein synthesis required for sustained axon regeneration. Reactivating the mTOR pathway by silencing either PTEN or TSC1 in adult neurons induces extensive axon regeneration, suggesting that retaining active protein synthesis in axotomized mature neurons is sufficient to initiate a neuronal regenerative program for axon regrowth. These findings highlight the importance of the mTOR pathway in determining the intrinsic axon-regrowth responsiveness of injured CNS neurons. The study also shows that activation of the mTOR pathway is sufficient to promote both RGC survival and axon regeneration. These results suggest that targeting the mTOR pathway could be a therapeutic approach to promote axon regeneration after CNS injury.A major obstacle to functional recovery after central nervous system (CNS) injury is the failure of axons to regenerate. This is due to both an inhibitory extrinsic environment and a diminished intrinsic regenerative capacity of mature CNS neurons. Removing extracellular inhibitory molecules only allows limited axon regeneration. This study shows that modulating the PTEN/mTOR pathway can promote axon regeneration in adult retinal ganglion cells (RGCs) after optic nerve injury. Deletion of PTEN, a negative regulator of the mTOR pathway, in adult RGCs promotes robust axon regeneration. This is because mTOR activity is suppressed in axotomized RGCs, impairing new protein synthesis and contributing to regeneration failure. Reactivating the mTOR pathway by conditional knockout of tuberous sclerosis complex 1 (TSC1) also leads to axon regeneration. These results suggest that manipulating intrinsic growth control pathways can promote axon regeneration after CNS injury. PTEN deletion activates the PI3K/mTOR pathway, which controls cell growth and size by regulating cap-dependent protein translation. This pathway is suppressed in axotomized adult neurons, limiting new protein synthesis required for sustained axon regeneration. Reactivating the mTOR pathway by silencing either PTEN or TSC1 in adult neurons induces extensive axon regeneration, suggesting that retaining active protein synthesis in axotomized mature neurons is sufficient to initiate a neuronal regenerative program for axon regrowth. These findings highlight the importance of the mTOR pathway in determining the intrinsic axon-regrowth responsiveness of injured CNS neurons. The study also shows that activation of the mTOR pathway is sufficient to promote both RGC survival and axon regeneration. These results suggest that targeting the mTOR pathway could be a therapeutic approach to promote axon regeneration after CNS injury.