Stress-dependent regulation of cardiac action potential duration is mediated by the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis. It is accompanied by increased slow outward potassium ion current, IKs . KCNQ1 and KCNE1 subunits co-assemble to form the IKs channel. The stress induced glucocorticoids could enhance KCNE1/KCNQ1 activity at least in part through upregulation of the serum- and glucocorticoid-inducible kinase 1 (SGK1). Mutations in either KCNE1 and/or KCNQ1 subunits cause long QT syndrome (LQTS), an inherited cardiac arrhythmia associated with increased risk of sudden cardiac death. Here we demonstrate that the exocytosis and endocytosis of KCNQ1/KCNE1 to/from the plasma membrane require specific small RAB-GTPases. We further demonstrate that RAB-dependent KCNQ1/KCNE1 exocytosis could be enhanced by SGK1, an effect involving the phospholipids PIP2. Identification of the RAB dependent IKs recycling pathway and its modulation by SGK1-PIP2 provides mechanistic insights into stress-induced acceleration of cardiac repolarization.