In the current study, we explored the axon regenerative approach to treat MS in mouse model and showed that targeted knock-out (KO) of axon growth inhibitory Krüppel-like factor 4 (Klf4) gene in RGCs of experimental autoimmune encephalomyelitis (EAE) mice is efficient in preventing not only the EAE-mediated RGC death but also restoring the function of injured axons by facilitating regeneration, and thereby improving the visual function in the mice even after the onset of EAE-mediated visual defects. This evidence concerns the gene KLF4 and experimental autoimmune encephalomyelitis.