SLC2A1 encodes GLUT1, a facilitative glucose transporter responsible for constitutive glucose uptake across cell membranes 12. GLUT1 possesses broad substrate specificity, transporting aldoses including pentoses and hexoses 34. Its most critical physiological role is mediating energy-independent glucose transport across the blood-brain barrier, serving as the brain's primary energy carrier 1. SLC2A1 mutations cause GLUT1 Deficiency Syndrome (GLUT1DS), a treatable neurological disorder characterized by impaired glucose transfer into the central nervous system, with emerging data revealing complex pathomechanisms beyond simple energy depletion 5. SLC2A1 variants are associated with epilepsy and type 2 diabetes with nephropathy 67. In cancer biology, SLC2A1 upregulation drives pathogenic metabolic and immunological changes. METTL3-mediated stabilization of SLC2A1 mRNA promotes colorectal cancer glycolysis and tumorigenesis 8. In lung squamous cell carcinoma, elevated GLUT1 expression associates with worse survival, poor immunotherapy response, and promotes macrophage polarization toward immunosuppressive M2 phenotype 9. Importantly, tumor-associated macrophage-specific SLC2A1 expression spatially excludes CD8+ T cells and drives checkpoint blockade resistance, making TAM-specific SLC2A1 inhibition a promising immunotherapeutic target 10. SLC2A1 also functions in ferroptosis regulation relevant to acute kidney injury 11.