KCNJ3 encodes Kir3.1, a G-protein-coupled inwardly rectifying potassium channel that permits preferential potassium influx into cells 12. The channel is characterized by voltage dependence regulated by extracellular potassium concentration, with inward rectification primarily mediated by internal magnesium blockade of outward current. KCNJ3 combines with KCNJ5-encoded Kir3.4 to form the acetylcholine-activated IKACh channel, which plays a critical role in cardiac electrophysiology 3. In disease pathophysiology, gain-of-function KCNJ3 mutations (p.N83H) cause hereditary bradyarrhythmias, sinus node dysfunction, and atrial fibrillation through increased basal IKACh channel current 3. Conversely, loss-of-function de novo variants (p.Leu333Ser, p.Arg313Gln) in the C-terminal domain are associated with early-onset epilepsy, suggesting KCNJ3's role in neuronal excitability 4. In pain homeostasis, the GPR37L1 ligand maresin 1 enhances KCNJ3-mediated potassium influx in satellite glial cells, promoting resolution of chemotherapy-induced neuropathic pain 5. Additionally, elevated KCNJ3 expression correlates with lymph node metastases and poor prognosis in breast cancer 6, with alternative splicing producing dominant-negative isoforms in cancer cells 7. These findings establish KCNJ3 as a multifunctional ion channel with implications for cardiac arrhythmias, neurological disorders, pain syndromes, and oncology.