SLC1A3 encodes EAAT1 (excitatory amino acid transporter 1), a sodium-dependent, high-affinity glutamate transporter that plays crucial roles in maintaining glutamate homeostasis in the central nervous system 1. The protein mediates uptake of L-glutamate, L-aspartate, and D-aspartate through a symporter mechanism that co-transports amino acids with sodium ions while counter-transporting potassium 1. This transporter is essential for removing glutamate from synaptic clefts, preventing excitotoxicity that can damage neurons 1. SLC1A3 is primarily expressed in astrocytes and plays critical roles in various neurological conditions. Mutations in SLC1A3 cause episodic ataxia type 6 (EA6), a dominantly inherited disorder characterized by transient episodes of incoordination and truncal instability triggered by physical exertion or emotional stress 23. Beyond its classical transport function, SLC1A3 has emerged as a biomarker in multiple diseases, showing upregulation in diabetic nephropathy where it clusters in endothelial cells and correlates with renal function deterioration 4. The gene is also implicated in Alzheimer's disease pathogenesis, where microglial SLC1A3 expression increases glutamine metabolism and enhances amyloid-β clearance 56. Additionally, SLC1A3 contributes to glutamine uptake in colorectal cancer progression 7.