SLC6A9 encodes glycine transporter 1 (GlyT1), a sodium- and chloride-dependent transporter that removes glycine from synaptic clefts and regulates both inhibitory and excitatory neurotransmission 1. The transporter operates through a conformational cycle involving outward-facing, occluded, and inward-facing states to facilitate glycine uptake 1. GlyT1 plays a crucial role in modulating NMDA receptor function by controlling glycine availability, making it a therapeutic target for schizophrenia treatment 12. Disease-causing variants in SLC6A9 reduce glycine-uptake activity, leading to increased extracellular glycine levels and aberrant glycinergic neurotransmission 3. These functional defects cause adolescent idiopathic scoliosis through disrupted spinal neural coordination and central pattern generator dysfunction 3. Additionally, SLC6A9 variants are associated with essential hypertension 4 and suicide attempt risk 5. The transporter also facilitates glycine uptake for glutathione synthesis in multiple myeloma cells, where blocking its function disrupts tumor progression 6. Clinical significance includes its role as a drug target, with several inhibitors in development for cognitive enhancement in schizophrenia, and its involvement in bone metabolism through glycine-dependent osteogenesis regulation 7.