Originally discovered as a tumor suppressor,7 PTEN deletion has been recently shown to dramatically increase postembryonic regeneration after injury in RGCs and corticospinal neurons in the CNS70,71 and axon outgrowth in the PNS.72 Loss of PTEN likely results in phosphatidylinositol (3,4,5)-trisphosphate (PIP3) accumulation, deregulation of AKT signaling, and likely increases regeneration through multiple downstream signaling effectors (for recent review see Ref. The gene discussed is PTEN; the disease is neoplasm.