We found that Netrin-1 over-expression after stroke promoted axonal outgrowth and regeneration by up-regulating the expression level of GAP-43, NF-200, and MAP-2 and that the suppression of the JNK1/c-Jun pathway reduced the expression of GAP-43 and NF-200 but did not affect the protein level of MAP-2. Here, JUN is linked to stroke disorder.