Another recent finding that stresses the potential role of astrocytic abnormalities in the expression of absence seizures is the selective induction of IL-1β in activated astrocytes within the cortical “initiation site” of absence seizures (i.e., the peri-oral region of the somatosensory cortex) (Fig. 5), but not in other cortical regions or in the thalamus of GAERS prior to seizure onset (Akin and others 2011). The gene discussed is IL1B; the disease is juvenile absence epilepsy.