The study investigates the role of intrinsic mechanisms in promoting axon regeneration in the adult central nervous system (CNS). The authors used a virus-assisted conditional knockout approach to delete PTEN, a negative regulator of the mammalian target of rapamycin (mTOR) pathway, in adult retinal ganglion cells (RGCs). They found that deleting PTEN significantly increased neuronal survival and robust axon regeneration after optic nerve injury. The mTOR pathway was suppressed in wild-type adult RGCs, impairing new protein synthesis and contributing to regeneration failure. Reactivating the mTOR pathway by conditional knockout of tuberous sclerosis complex 1 (TSC1), another negative regulator of mTOR, also led to axon regeneration. These findings suggest that manipulating intrinsic growth control pathways, such as the mTOR pathway, could be a therapeutic approach to promote axon regeneration after CNS injury.The study investigates the role of intrinsic mechanisms in promoting axon regeneration in the adult central nervous system (CNS). The authors used a virus-assisted conditional knockout approach to delete PTEN, a negative regulator of the mammalian target of rapamycin (mTOR) pathway, in adult retinal ganglion cells (RGCs). They found that deleting PTEN significantly increased neuronal survival and robust axon regeneration after optic nerve injury. The mTOR pathway was suppressed in wild-type adult RGCs, impairing new protein synthesis and contributing to regeneration failure. Reactivating the mTOR pathway by conditional knockout of tuberous sclerosis complex 1 (TSC1), another negative regulator of mTOR, also led to axon regeneration. These findings suggest that manipulating intrinsic growth control pathways, such as the mTOR pathway, could be a therapeutic approach to promote axon regeneration after CNS injury.