SLC1A2 encodes EAAT2 (excitatory amino acid transporter 2), the predominant glutamate transporter in the human brain that functions as a sodium-dependent, high-affinity transporter for L-glutamate, L-aspartate, and D-aspartate 1. EAAT2 operates as a symporter, transporting one amino acid molecule with 2-3 Na+ ions and one proton while counter-transporting one K+ ion, and mediates chloride flux to prevent charge accumulation 1. Beyond its classical neuronal role in glutamate clearance from synaptic clefts, EAAT2 functions in diverse cellular contexts including astrocytes where it regulates glutamate homeostasis and social memory 2, and in macrophages where it supports inflammatory responses through lysosomal amino acid efflux and mTORC1 activation 3. Disease-associated SLC1A2 variants cause developmental and epileptic encephalopathy with variable severity correlating with transporter dysfunction 14. EAAT2 dysfunction contributes to frontotemporal dementia pathogenesis through astroglial toxicity and synaptic degeneration 5. Additionally, cancer cells exploit EAAT2 disruption to hijack neurometabolic coupling and promote brain metastasis 6. The transporter's diverse roles make it a potential therapeutic target for neurological disorders, metabolic diseases, and cancer.