In GAT-1 knockout mice, spontaneous spike–wave discharges and absence seizures are observed as the result of an increased tonic inhibition due to an increase of GABA in the extracellular cleft due to defective GAT-1 function (Richards et al., 1995; Belelli et al., 2009; Cope et al., 2009). Here, SLC6A1 is linked to juvenile absence epilepsy.