Since its initial description¹ seven decades ago, the Wolff–Parkinson–White syndrome has attracted cardiologists' attention not only because of its clinical importance but also because of the opportunity it provides to learn about electrical conduction in the heart. Yet, until the report by Gollob and colleagues in this issue of the Journal, ² the molecular basis of the syndrome remained a mystery. The Wolff–Parkinson–White syndrome affects 1 to 3 persons per 1000.²,³ These persons are born with an abnormal electrical connection, termed an accessory pathway or bypass tract, between the atria and ventricles. Because accessory pathways often have a more rapid . . .