SLC39A2 (ZIP2) is a zinc transporter that mediates the facilitated diffusion of divalent cations, primarily zinc (Zn2+), across the plasma membrane into cells 1. The transporter exhibits substrate selectivity in the order Zn2+ > Cd2+ ≥ Cu2+ > Co2+, with its activity modulated by extracellular pH and membrane potential rather than H+ driving force 12. Structurally, SLC39A2 contains a single divalent metal-binding site with key residues including Glu-179, His-175, His-202, and Glu-276 coordinating substrate binding 2. SLC39A2 exhibits highly cell-type-specific and developmentally regulated expression, particularly in pericentral hepatocytes, developing keratinocytes, and immature dendritic cells 3. The transporter plays critical roles in zinc homeostasis during dietary deficiency and pregnancy, and influences iron and calcium homeostasis in developing embryos 3. In wound healing, SLC39A2 expression is downregulated during reepithelialization, associating with epidermal maturation 4. Recently, SLC39A2 upregulation was identified as a mechanism in intestinal inflammation; suppressing Slc39a2 expression via miR-5106 delivery restored zinc homeostasis and reduced neutrophil extracellular trap formation in colitis models 5. Additionally, SLC39A2 polymorphisms (rs2234636) were associated with increased arsenic-related bladder cancer susceptibility in high-exposure populations 6.