SLC44A1 encodes a choline/H+ antiporter that mediates Na+-independent choline transport across cell membranes 1. Beyond choline, SLC44A1 functions as a high-affinity ethanolamine/H+ antiporter, regulating extracellular ethanolamine supply for the CDP-ethanolamine pathway and balancing the Kennedy pathway's phosphatidylcholine and phosphatidylethanolamine arms 2. The transporter is enriched in oligodendrocytes and is essential for CNS myelination; SLC44A1 deficiency impairs oligodendroglial maturation and phospholipid biosynthesis, disrupting myelin lipid composition 3. Clinically, SLC44A1 mutations cause childhood-onset neurodegeneration featuring cerebellar atrophy, leukoencephalopathy, and cognitive decline 4. Importantly, citicoline supplementation restores developmental myelination in SLC44A1-deficient models, suggesting a potential therapeutic approach 3. Additionally, SLC44A1-PRKCA chr9 fusions characterize papillary glioneuronal tumors, a rare CNS neoplasm, serving as a specific diagnostic marker 5. In cancer, elevated SLC44A1 expression enables tumor cells to compete with immune cells for choline, promoting immune evasion and tumor-associated macrophage repolarization 6. Thus, SLC44A1 plays critical roles in membrane synthesis, neuronal development, and immune regulation.