In particular, the correction of the trafficking of KCNH2 (LQTS2) potassium channel through intracellular mechanisms restored hERG currents and reduced arrhythmia in LQTS2 patient-derived cardiomyocytes, also documenting the usefulness of iPSC-cardiomyocytes in LQTS2 modeling and drug testing. This evidence concerns the gene KCNH2 and cardiac arrhythmia.