KCNJ2 encodes Kir2.1, an inward rectifier potassium channel that preferentially allows potassium influx over efflux 1. The channel's voltage dependence is regulated by extracellular potassium concentration, with inward rectification primarily mediated by intracellular magnesium blockade of outward current 2. KCNJ2 establishes action potential waveform and excitability in neuronal and muscle tissues 3, and regulates membrane repolarization during cardiac muscle action potentials [GO annotation]. Beyond electrophysiology, KCNJ2-mediated membrane hyperpolarization promotes hair growth by enhancing dermal fibroblast Wnt signaling and reducing intracellular calcium 4, and controls nutrient acquisition in macrophages by facilitating nutrient transporter cell-surface retention 5. Mutations in KCNJ2 cause Andersen-Tawil syndrome, characterized by periodic muscle paralysis, cardiac repolarization abnormalities, and physical dysmorphisms 6. KCNJ2 variants are associated with atrial fibrillation and long QT syndrome, though evidence for the latter as a definitive cause is limited 7. Therapeutically, KCNJ2 overexpression prevents arrhythmias in transplanted stem cell-derived cardiomyocytes 8, while KCNJ2 inhibition reduces atrial fibrillation susceptibility via CREB signaling suppression 9.