SLC41A1 encodes a Na+/Mg2+ exchanger that functions as the predominant Mg2+ efflux system at the plasma membrane 1. Transport activity is driven by the inwardly directed Na+ electrochemical gradient, making it dependent on extracellular Na+ concentration 1. The exchanger is ubiquitously expressed and regulated through phosphorylation by protein kinase A 1. SLC41A1 is essential for systemic magnesium homeostasis; zebrafish slc41a1 knockdown results in renal Mg2+ wasting and decreased whole-organism Mg2+ content 2. At the cellular level, SLC41A1 facilitates circadian Mg2+ fluxes that regulate clock-controlled gene expression and metabolism 3. Dysregulation of SLC41A1 has clinical significance: null mutations cause nephronophthisis-like nephropathy 2 4, and SLC41A1 variants are associated with Parkinson's disease susceptibility 5, with specific polymorphisms showing reduced PD risk in Iranian populations 6. Recent evidence demonstrates that inflammatory stimuli (e.g., LPS) can upregulate SLC41A1 through STAT5A, leading to pathological Mg2+ depletion, mitochondrial dysfunction, and cell death in dental stem cells 7. Additionally, SLC41A1 overexpression correlates with hepatocellular carcinoma progression and immune dysregulation 8.