SLC30A7 (ZNT7) is a zinc ion transporter that mediates zinc entry from the cytosol into organelles along the secretory pathway, particularly the Golgi apparatus 12. By regulating intracellular zinc homeostasis, SLC30A7 contributes to the activation and folding of zinc-dependent enzymes like alkaline phosphatases 12. Biallelic SLC30A7 variants cause Ziegler-Huang syndrome, characterized by stunted growth, testicular hypoplasia, and bone marrow failure 3. Heterozygous de novo variants have been identified in Joubert syndrome cases, suggesting additional roles in neuronal development, possibly through interactions with ciliary proteins and Sonic Hedgehog signaling 4. SLC30A7 also functions in glucose metabolism, as Slc30a7 deletion impairs glucose tolerance and reduces glucose-stimulated insulin secretion in mice 5. Recent studies reveal broader pathophysiological roles: SLC30A7 regulates cuproptosis (copper-dependent cell death) in glioblastoma via the JAK2/STAT3/ATP7A pathway 6, and miR-200c-3p suppresses SLC30A7 to regulate pyroptosis in diabetic retinopathy 7. Downregulation of SLC30A7 correlates with increased risk of diabetic peripheral artery disease 8. Genetic variants in SLC30A7 contribute to multiple sclerosis susceptibility 9.