SLC1A6 encodes EAAT4, a sodium-dependent, high-affinity glutamate transporter that mediates the uptake of L-glutamate, L-aspartate, and D-aspartate by coupling the transport of one amino acid molecule with two or three Na+ ions and one proton, while counter-transporting one K+ ion 1. The transporter also mediates chloride flux uncoupled from amino acid transport, preventing negative charge accumulation 2. SLC1A6 plays a redundant role in rapidly removing glutamate from synaptic clefts, essential for terminating postsynaptic glutamate action. Clinically, SLC1A6 variants are associated with schizophrenia susceptibility; polymorphisms in SLC1A6 show significant association with schizophrenia in Japanese populations 3, and NRG1 risk genotypes correlate with decreased SLC1A6 expression in cerebellar regions 4. A genome-wide association study identified SLC1A6 variants (rs112501869) associated with normal hearing function at 0.25 kHz 5. In cancer, elevated SLC1A6 expression in bladder cancer promotes resistance to immunotherapy by suppressing CD8+ T cell effector function and reducing immune infiltration; SLC1A6 knockdown enhances immunotherapy efficacy 6. SLC1A6 has also been identified as an independent prognostic predictor in bladder cancer survival models 7. Genetic variations in SLC1A1 (not SLC1A6) associate with posttraumatic seizure risk following traumatic brain injury 8.