KCNJ4 encodes Kir2.3, an inward rectifier potassium channel that preferentially allows potassium flow into cells, with voltage dependence regulated by extracellular potassium concentration and blockade of outward current mediated by internal magnesium [UniProt]. The channel localizes to the basolateral plasma membrane and exhibits PDZ domain binding capacity [GO Annotations]. In cardiac physiology, KCNJ4 expression is dynamically regulated during atrial myocardium cultivation, showing downregulation after 12 days in culture 1. Notably, KCNJ4 expression is reduced in male hearts at sudden cardiac death compared to nonarrhythmic deaths, suggesting sex-specific ion-channel dysregulation contributes to arrhythmic vulnerability 2. Beyond cardiology, KCNJ4 has emerged as clinically significant in multiple disease contexts. In lung adenocarcinoma, KCNJ4 overexpression correlates with cancer progression, shorter overall survival, and independent prognostic significance; KCNJ4 silencing suppresses proliferation, migration, and invasion via MEK/ERK pathway inhibition 3. KCNJ4 variants cause refractory epilepsy through both gain-of-function and loss-of-function mechanisms affecting potassium current amplitude 4. Additionally, KCNJ4 overexpression protects against mycotoxin-induced damage by regulating cell cycle and mitochondrial function 5. KCNJ4 responds to viral infection and dietary polyphenols, demonstrating broader cellular regulation 6, 7, and altered expression in neurodevelopmental disorders 8.