SLC30A9 (solute carrier family 30 member 9) is a mitochondrial proton-coupled zinc ion antiporter that mediates zinc export from mitochondria and maintains intracellular zinc homeostasis 1. The protein is evolutionarily conserved and coevolves with oxidative phosphorylation machinery 2. SLC30A9 is critical for mitochondrial integrity and function; its loss impairs mitochondrial complex I activity, membrane potential, and ATP production while disrupting mitochondrial morphology 31. In mammals, germline SLC30A9 loss causes midgestational lethality with severe developmental abnormalities, while brain-specific knockout results in dwarfism and growth hormone/IGF-1 pathway dysfunction 3. Pathogenic SLC30A9 variants cause Birk-Landau-Perez syndrome, an autosomal recessive disorder characterized by progressive hyperkinetic movement disorder, oculomotor apraxia, and ptosis 4. Beyond mitochondrial functions, SLC30A9 acts as a nuclear coactivator for transcriptional regulation of Wnt-responsive genes. Dysregulation of SLC30A9 contributes to cervical cancer and diffuse large B-cell lymphoma progression through enhanced mitochondrial hyperfunction and altered metabolic signaling 56. Emerging evidence links SLC30A9 variants to severe diabetic retinopathy in type 1 diabetes 7, suggesting broader metabolic disease relevance.