SLC37A3 is a solute carrier family member localized to the endoplasmic reticulum and lysosomal membranes 1, though unlike other SLC37 family members, it lacks glucose-6-phosphate antiporter activity 2. Its primary characterized function is forming a transporter complex with ATRAID in osteoclasts to facilitate the cytosolic release of nitrogen-containing bisphosphonates (N-BPs) that have accumulated in lysosomes via fluid-phase endocytosis 3. This mechanism is critical for N-BP action in treating bone diseases like osteoporosis. Beyond this established role, SLC37A3 may be involved in glucose metabolism regulation and cellular metabolic reprogramming. In glioblastoma, SLC37A3 expression is upregulated under hypoxia via HIF-1α signaling and correlates with cancer stem cell phenotypes and reduced neurosphere size when silenced 4. In hepatocellular carcinoma, elevated SLC37A3 expression associates with poor prognosis, advanced tumor stages, and increased cell proliferation and metastasis 5. Importantly, SLC37A3 mutations cause retinitis pigmentosa, a rod-cone dystrophy presenting with night blindness and progressive photoreceptor degeneration 6, though the molecular mechanism in retinal tissue remains unclear. These diverse disease associations suggest SLC37A3 participates in multiple metabolic pathways beyond its characterized N-BP transport function.