SLC30A10 is a calcium:manganese antiporter located at the plasma membrane that mediates manganese efflux coupled to calcium influx, functioning as the primary mechanism for manganese homeostasis 1. The transporter is essential for preventing intracellular manganese accumulation, as excessive manganese induces oxidative stress, mitochondrial dysfunction, and apoptosis 1. SLC30A10 may also function as a zinc ion transporter, regulating intracellular zinc homeostasis 2. Transcriptional regulation of SLC30A10 occurs through hypoxia-inducible factors (HIF), where elevated manganese activates HIF1α/HIF2α to upregulate SLC30A10 expression while simultaneously inducing NR4A1, which represses SLC30A10 to prevent manganese deficiency 3. The transporter contains a critical manganese-binding site at aspartate 40 (D40), with disease-associated mutations at this residue abolishing transport function 4. Bi-allelic SLC30A10 mutations cause hypermanganesemia with dystonia 1 (HMNDYT1), characterized by progressive dystonia with disease onset typically around 2.5 years of age, alongside liver disease and polycythemia 15. Common polymorphisms, particularly T95I, may influence manganese neurotoxicity susceptibility, though functional studies suggest this variant retains near-normal transporter activity 67. Early diagnosis through blood manganese levels and brain MRI enables timely therapeutic intervention 1.