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The EED\u2010containing polycomb repressive complex 2 (PRC2) catalyzes histone H3K27 methylation and represses key nerve repair genes such as<jats:italic>Shh<\/jats:italic>,<jats:italic>Gdnf<\/jats:italic>, and<jats:italic>Bdnf<\/jats:italic>, and their activation is accompanied by loss of H3K27 methylation. Analysis of nerve injury in mice with a Schwann cell\u2010specific loss of EED showed the reversal of polycomb repression is required and a rate limiting step in the increased transcription of<jats:italic>Neuregulin 1<\/jats:italic>(type I), which is required for efficient remyelination. However, mouse nerves with EED\u2010deficient Schwann cells display slow axonal regeneration with significantly low expression of axon guidance genes, including<jats:italic>Sema4f<\/jats:italic>and<jats:italic>Cntf.<\/jats:italic>Finally, EED loss causes impaired Schwann cell proliferation after injury with significant induction of the<jats:italic>Cdkn2a<\/jats:italic>cell cycle inhibitor gene. Interestingly, PRC2 subunits and<jats:italic>CDKN2A<\/jats:italic>are commonly co\u2010mutated in the transition from benign neurofibromas to malignant peripheral nerve sheath tumors (MPNST's). 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