Glial activation and oxidative stress [5], [6] might further promote the hyperexcitability in Cstb−/− mice, as glial derived proinflammatory chemokines and cytokines, highly expressed also in P30 Cstb−/− mice, have been found to reduce the seizure threshold and may thus contribute to recurrent excitation in epilepsy [48]. This evidence concerns the gene CSTB and epilepsy.