The increased INaL, in addition to prolonging APD, also elevates intracellular Na+ concentration which in turn activates CaMKII and slows Ca2+ extrusion from the cells via the sodium–calcium exchanger (NCX) leading to increased sarcoplasmic (SR) Ca2+ content, and this can elicit delayed afterdepolarization (DAD) and consequent arrhythmias [65]. This evidence concerns the gene CAMK2G and Arrhythmia.