In particular, a targeted mutation analysis has linked the Long-QT Syndrome (LQTS) to a single missense mutation in AKAP9, which disrupts its binding to a slowly activating cardiac potassium channel (IKs), thus preventing proper cAMP-dependent regulation of the latter, and leading to delayed repolarization of the ventricular action potential (Chen et al., 2007). This evidence concerns the gene AKAP9 and familial long QT syndrome.