SLC6A11 encodes GAT-3 (GABA transporter 3), a sodium- and chloride-dependent transporter mediating GABA reuptake from the synaptic cleft 1. The transporter operates with a 3 Na+:1 Cl-:1 GABA coupling stoichiometry and maintains GABA homeostasis in the central nervous system 2. SLC6A11 is expressed in astrocytes and other neural tissue, contributing to both synaptic and extrasynaptic GABA regulation 3. Dysfunction of SLC6A11 is implicated in multiple neurological disorders. Haploinsufficient deletions of SLC6A11 in 3p- syndrome cause epilepsy with characteristic EEG abnormalities, including myoclonic or absence seizures with generalized high-amplitude slow waves 4. The therapeutic agent 4-phenylbutyrate (PBA) restored GABA uptake and reduced seizure burden in patients with SLC6A11 deletions 5. Genetic variants (rs2304725) increase epilepsy susceptibility 3-fold and are associated with drug-resistant epilepsy 6. Additionally, SLC6A11 polymorphisms contribute to tardive dyskinesia risk in schizophrenic patients through GABAergic pathway dysfunction 7. These findings establish SLC6A11 as a critical regulator of GABAergic neurotransmission and a promising therapeutic target for seizure disorders and movement complications.