The hypothesis that regenerative failure of axons in the adult mammalian CNS is due to release of a growth inhibitor from injured oligodendrocytes and/or myelin2, predicts that regeneration of injured fibers would proceed unchecked in unmyelinated CNS regions. This prediction was borne out by observations on the stratum opticarum of the mouse retina. Axonal sprouts, first seen 14-16 h post-lesion (pl), continued growing until at least 100 days pl, well beyond the time at which regeneration fails in myelinated CNS regions.