Epilepsy is generally viewed as resulting from an unbalanced excitatory/ inhibitory drive, where either excitatory transmission is enhanced and/or inhibitory transmission is decreased. However, studies in genetic and pharmacological models of non-convulsive typical absence seizures have revealed that an increased activation of extrasynaptic γ-aminobutyric acidA (GABAA) receptors (eGABAARs), and the resulting enhanced tonic GABAA inhibition in thalamocortical (TC) neurons, is a necessary and sufficient condition for the expression of these seizures. Importantly, in genetic absence models, the mechanism underlying eGABAAR gain of function is non-neuronal in nature as it results from a malfunction in the thalamic astrocytic GABA transporter, GAT-1. These results challenge the existing view that typical absence seizures are underpinned by a widespread loss of GABAergic function in TC circuits, and are supported by the evidence that drugs that increase GABAergic signalling elicit or aggravate absence seizures in animal model and humans. Furthermore, by highlighting a vital role for astrocytes and eGABAARs in the pathophysiology of typical absence epilepsy, these new findings offer novel targets for the development of more effective anti-absence drugs.