The failure of axon regeneration after CNS injury is due to an inadequate or inappropriate regenerative response from damaged CNS axons and to a CNS environment that inhibits regeneration. This inhibitory environment contains many molecules that promote axon growth as well as molecules that inhibit it, but the balance of activities in the damaged CNS does not favour the regeneration of adult CNS axons. In principle, therefore, axon regeneration could be achieved in three ways:(1) Inhibitory molecules might be destroyed or blocked,(2) the amount of permissive molecules might be increased, or new permissive molecules introduced,(3) Axons might be altered so that they can grow in the inhibitory CNS environment. Some success has been achieved with all three of these approaches. This review addresses the inhibitory properties of the glial scar, a structure which forms wherever the CNS is damaged, and which is one source of axon growth inhibitory molecules in CNS inju-