SLC31A1 (solute carrier family 31 member 1) is a copper transporter that mediates copper ion influx across cell membranes and mobilizes copper from endosomal compartments 1. As the major mammalian copper influx transporter, SLC31A1 plays critical roles in maintaining cellular copper homeostasis, which is essential for metalloenzyme function and metabolic regulation 1. Mechanistically, SLC31A1 transports copper(1+) ions across the plasma membrane and facilitates copper mobilization from intracellular compartments, making copper bioavailable for enzyme cofactor incorporation and cellular signaling 2. Copper availability regulated by SLC31A1 influences multiple cellular processes including mitochondrial metabolism, autophagy, cell death pathways, and immune regulation 3. In cardiac pathology, SLC31A1 downregulation causes mitochondrial copper depletion, enhances glycolysis, and promotes cardiac fibrosis through epigenetic mechanisms involving MeCP2-mediated transcriptional suppression 2. In cancer, SLC31A1 upregulation correlates with worse overall survival in breast, cervical, head and neck, and esophageal cancers 4. SLC31A1 promotes cancer immune evasion by facilitating copper-dependent PD-L1 expression in tumor cells, and copper chelators that inhibit SLC31A1 function enhance anti-tumor immunity 5. Clinically, SLC31A1 represents a potential diagnostic and prognostic biomarker across multiple cancer types and a therapeutic target for cancer immunotherapy enhancement 46.