Purpose: P27kip1 is well-known as a cell cycle inhibitor and also plays an important role for cell differentiation. We hypothesized that if we caused retinal degeneration in a p27(-/-) mouse, then the appropriate method of restoration may be different from that of wild mice and therefore suggest a therapeutic methodology for retinal regeneration. Methods: Histological and electrophysiological (ERG) examination was performed on p27(-/-) mice retina. We injected N-methy-N-nitrosourea (MNU) to induce retinal degeneration. BrdU was used to identify the dividing cells in the retina. Results: Thicker retina were observed in the p27(-/-) mice when compared to those of the p27(-/+) mice or wild type mice. Almost all retinal layers were thick and optic nerves were also enlarged. A statistically significant decrease of a and b waves amplitudes of ERG was observed in p27(-/-) mice when compared to those of the other mice. BrdU and nestin positive cells were present at the outer nuclear layer with no difference between p27(-/-) and wild type mice after MNU injection. Conclusion: p27(-/-) mice showed thicker retina and less retinal function than those of other mice. The MNU-induced retinal degeneration in p27(-/-) mice closely resembled the reaction of the other mice with no retinal regeneration observed in our experimental condition.