The cAMP level was also increased in glioblastoma cells when they were treated with synthetic AM1-52 [302]; AM favored c-Jun and c-Jun N-terminal kinase (JNK) phosphorylation in glioblastoma cells, and the suppression of c-Jun expression or the inhibition of JNK activation impaired the actions mediated by AM on cyclin D1 and cell proliferation [219]. This evidence concerns the gene JUN and glioblastoma.