At least 16 distinct congenital long QT syndromes are now recognized as a result of mutations in multiple voltage-gated K, Ca, and Na channel genes, but interestingly also as a result of mutations in non-channel genes, including those for Ankyrin (ANK2, LQT4), A-kinase anchor protein (AKAP9, LQT1), and alpha-1 syntrophin (SNTA1, LQT12).3 Such findings indicate a synergy with the ion channel substrate, and can spur further insights to molecular complexes and convergent signaling pathways. This evidence concerns the gene SNTA1 and Prolonged QT interval.