SLC2A5 encodes GLUT5, a fructose-selective transporter essential for dietary fructose absorption in the small intestine. The protein mediates fructose uptake across cell membranes with minimal activity toward other monosaccharides, though it can transport 2-deoxyglucose with low efficiency. Beyond nutrient absorption, SLC2A5 plays a regulatory role in salt handling and blood pressure responses to dietary fructose. In disease contexts, SLC2A5 expression is frequently elevated in cancer cells, where fructose metabolism supports tumor angiogenesis and metastatic progression 12. GLUT5-expressing endothelial cells metabolize fructose via AMPK-dependent pathways to fuel mitochondrial respiration and enhance vessel growth 1. At the cellular level, SLC2A5 inactivation inhibits cancer cell migration and metastasis across multiple tumor models 2. Recent work reveals that high fructose exposure during early life suppresses microglial phagocytosis through SLC2A5-dependent fructose uptake and metabolic rewiring, linking fructose metabolism to neurodevelopmental impairment and adolescent anxiety 3. Clinical applications are emerging: engineered immune cells expressing GLUT5 demonstrate enhanced anti-tumor efficacy in glucose-limited tumor microenvironments 4, and histone deacetylase inhibitors that suppress SLC2A5 expression sensitize colon cancer cells to platinum compounds 5. Genome-wide association studies identify SLC2A5 as a potentially druggable immunometabolic target in critical COVID-19 6 and acute respiratory distress syndrome 7.