SLC6A11 encodes GAT3 (GABA transporter 3), a sodium- and chloride-dependent transporter that mediates gamma-aminobutyric acid (GABA) reuptake at the plasma membrane 1. The transporter operates via a 3 Na⁺:1 Cl⁻:1 GABA coupling stoichiometry and also transports beta-alanine and, to a lesser extent, taurine and guanidinoacetate. GAT3 is expressed in astrocytes and plays a critical role in GABA homeostasis in both synaptic and extrasynaptic brain regions 2. Haploinsufficient deletions of SLC6A11 cause impaired GABA uptake and contribute to epileptic phenotypes, particularly in 3p deletion syndrome where microdeletions affect both SLC6A1 and SLC6A11 34. Genetic variants in SLC6A11 are associated with increased epilepsy risk and altered antiepileptic drug response in Iraqi populations, with the TT genotype conferring a 3-fold increased risk 5. SLC6A11 polymorphisms have also been implicated in tardive dyskinesia susceptibility in schizophrenic patients 6. Recent evidence suggests that Rev-erbα regulates SLC6A11 expression as part of circadian control of GABAergic signaling and seizure susceptibility 7. For 3p-syndrome patients with SLC6A11 deletions, 4-phenylbutyrate (Ravicti) treatment showed promise in reducing seizures and improving motor function, though cognitive impairments persisted 3.