SLC31A2 (CTR2) is a copper transporter localized predominantly to late endosomal and lysosomal membranes 1. While it functions as a low-affinity copper(1+) importer in vitro, it does not serve as a primary copper importer in vivo; instead, it acts as a regulator of SLC31A1 (CTR1), facilitating cleavage or stabilization of truncated CTR1 forms to modulate endosomal copper export and cisplatin accumulation 2. As a component of the mammalian copper homeostasis network alongside ATP7A and ATP7B, SLC31A2 helps redistribute intracellular copper across cellular compartments in response to metabolic demands 3. Clinically, SLC31A2 dysregulation associates with multiple pathologies. In lung adenocarcinoma, SLC31A2 is part of a copper metabolism-related gene signature predicting patient survival and immunotherapy response 4. In melanoma, elevated SLC31A2 correlates with chemotherapeutic drug resistance across multiple agents 5. SLC31A2 variants, particularly the c.86C>T (p.S29L) mutation, show enriched frequency in Wilson disease patients, where CTR2-S29L increases intracellular copper accumulation and copper-induced apoptosis 6. Additionally, SLC31A2 expression level is incorporated into predictive models for immune checkpoint inhibitor efficacy in advanced non-small cell lung cancer 7, highlighting its emerging role as a cancer biomarker alongside its fundamental function in copper homeostasis.