Absence seizures (ASs) are genetic generalized seizures and one of the critical neurological phenotypes that originates from abnormalities in corticothalamic (CT) networks. Genetic analyses of cohorts with only ASs have identified 2p16.1 and 2q22.3 as significant loci and a few genes related to intrinsic and synaptic membrane channels. In normal animals, the genetic mutation of a single voltage- or ligand-gated channel in a single cortical or thalamic neuronal population can lead to spontaneous ASs. The electrographic activity of ASs invariably initiates from a localized cortical area but the full expression of these seizures’ clinical symptoms requires interactions between cortical and thalamic networks. In contrast to focal and other genetic generalized seizures, the ictal activity of cortical and thalamic neurons during ASs is predominantly characterized by a decreased, but highly synchronized, firing with individual neurons often showing a different firing pattern from one seizure to the next.. The high remittance rate of children with ASs indicates that CT networks, and/or their modulatory inputs from the basal ganglia and brain stem, have the inherent capacity to compensate for the developmental abnormalities that lead to ASs, but the mechanisms of remittance have not been investigated since all available models lack this feature of human ASs