Similarly, aberrations in growth or pituitary dysfunction have not been described in patients with the extremely rare short QT syndrome (27, 28), or familial atrial fibrilliation (29) due to activating KCNQ1 mutations, which also corroborates that the electrical activity of KCNQ1–KCNE channels may not be the primary mechanism underlying the KCNQ1-related pituitary dysfynction (4). This evidence concerns the gene KCNQ1 and Familial short QT syndrome.