In a systemic kainate rat epilepsy model, seizure induction was associated with a reduction in canonical Wnt signaling mediators Wnt1, beta-catenin, Dvl1, and phospho-GSK3b (inactive Wnt inhibitor) 72 h after injection; anti-epileptic drug treatment (carbamazepine) increased expression of these canonical Wnt signaling mediators and was associated with reduced neuronal death, as well as reduced glutamate excitotoxicity, implicating canonical Wnt signaling as a potential neuroprotective signaling pathway [31]. The gene discussed is DVL1; the disease is epilepsy.