SLC17A7 (VGLUT1) is a multifunctional transporter essential for glutamatergic neurotransmission. At synaptic vesicles, it functions primarily as a uniporter transporting L-glutamate from the cytoplasm into vesicles, driven by the proton electrochemical gradient established by vacuolar H+-ATPase 1. Additionally, SLC17A7 operates as a chloride channel and potassium/proton antiporter, regulating vesicular acidification and ionic gradients to maintain glutamate uptake 1. At the plasma membrane, it functions as a sodium-phosphate symporter for synaptic phosphate homeostasis 1. SLC17A7 is necessary for visual-evoked responses and synaptic transmission in glutamatergic neurons 1. Clinically, SLC17A7 dysfunction associates with multiple neuropsychiatric and neurodegenerative conditions. Genetic polymorphisms in SLC17A7 correlate with negative symptoms in schizophrenia 2. The gene is identified as a hub marker for early Alzheimer's disease, particularly in dysfunctional synaptic signaling 3. SLC17A7 is recognized as a bivalent tumor suppressor gene in glioblastoma, with downregulation correlating with increased cell proliferation and invasion 4. Additionally, SLC17A7 dysfunction is implicated in HIV encephalitis pathology 5 and represents a downregulated hub gene in glioma with diagnostic potential 6. Co-expression of SLC17A7 in excitatory neurons suggests roles in neurodevelopmental and neuropsychiatric disease mechanisms 7.