SLC1A6 encodes EAAT4, a high-affinity sodium-dependent glutamate transporter that mediates cellular uptake of L-glutamate, L-aspartate, and D-aspartate by co-transporting three sodium ions and one proton while counter-transporting one potassium ion. The transporter also conducts chloride flux uncoupled from amino acid transport, preventing charge accumulation during aspartate-sodium symport. SLC1A6 plays a redundant role in rapidly clearing glutamate from the synaptic cleft, essential for terminating postsynaptic glutamate signaling. Genetic variation in SLC1A6 has been associated with schizophrenia susceptibility; specific haplotypes showed significant association in a Japanese population 1, and cerebellar expression levels correlate with neuregulin-1 risk genotypes 2. A genome-wide association study identified SLC1A6 variants associated with normal hearing function thresholds at 0.25 kHz 3. In cancer, SLC1A6 expression promotes resistance to immune checkpoint inhibitors in bladder cancer patients receiving neoadjuvant immunotherapy 4. High SLC1A6 expression correlates with poor prognosis, disease progression, and reduced immune infiltration, and SLC1A6 knockdown enhanced CD8+ T cell effector function and improved immunotherapy efficacy in tumor models. SLC1A6 is an independent prognostic predictor in bladder cancer 5. Targeting SLC1A6 may improve responses to immunotherapy and represents a potential therapeutic strategy.