KCNQ1 (Kv7.1) is a voltage-gated potassium channel that functions as the pore-forming subunit of the slow delayed rectifier potassium current (IKs) in cardiac tissue 1. In the heart, KCNQ1 heterodimerizes with the beta subunit KCNE1 to mediate ventricular repolarization following action potentials 1. Channel gating is regulated through tissue-specific co-assembly with different KCNE beta subunits (KCNE1-5) and requires phosphatidylinositol-4,5-bisphosphate (PIP2) binding, which triggers conformational changes that dilate the pore gate 2. Beyond cardiac function, KCNQ1 regulates gastric acid secretion, salt homeostasis, and glucose metabolism 2. Loss-of-function KCNQ1 mutations cause Long QT syndrome type 1 (LQT1), characterized by prolonged QT intervals and arrhythmia risk, primarily during exercise 3. Homozygous mutations result in Jervell and Lange-Nielsen syndrome, combining cardiac arrhythmias with congenital deafness 4. Conversely, gain-of-function mutations cause Short QT syndrome with increased sudden death risk 5. Additionally, KCNQ1 polymorphisms (rs2237892, rs2237895) are associated with elevated type 2 diabetes susceptibility 6, though specific mechanistic links to glucose homeostasis require further clarification. KCNQ1-deficient cardiomyocytes demonstrate prolonged action potentials and irregular rhythms, providing models for studying pathogenic mechanisms and drug responses 7.