SLC39A14 (ZIP14) is an electroneutral membrane transporter mediating cellular uptake of divalent metal cations, primarily zinc, manganese, and iron, which are essential for tissue homeostasis and metabolism 123. The transporter functions as an energy-dependent symporter, transporting metal-bicarbonate complexes across the plasma membrane [UniProt]. SLC39A14 regulates intestinal zinc uptake critical for maintaining tight junctions and permeability, and controls insulin receptor signaling and glucose metabolism in hepatocytes through zinc-dependent intracellular processes 4. It serves as the major manganese transporter in intestinal epithelial cells and participates in blood-brain barrier manganese uptake 56. Additionally, SLC39A14 mediates non-transferrin-bound iron (NTBI) uptake and endosomal iron transport 78. Clinically, SLC39A14 dysfunction is associated with ferroptosis-related pathologies. SLC39A14 upregulation promotes hepatocyte ferroptosis in liver ischemia-reperfusion injury and cirrhosis 91011. In skeletal muscle aging, elevated SLC39A14 combined with declining transferrin receptor 1 drives labile iron accumulation and ferroptosis-mediated regeneration impairment 12. SLC39A14 also facilitates ferroptosis during acute lung injury 13. In cancer, SLC39A14 promotes zinc uptake by tumor cells, depleting the tumor microenvironment and impairing T cell immunity in nasopharyngeal carcinoma 14. These findings identify SLC39A14 as a therapeutic target for ferroptosis-related diseases and cancer immunotherapy.