The three most commonly associated genes are gain-of-function mutations in KCNH2, KCNQ1, and KCNJ2, which encode potassium channels (42-44); however, rare variants in these genes account for ~20% of SQTS cases, so the majority of SQTS cases are genetically unexplained (45). This evidence concerns the gene KCNQ1 and Familial short QT syndrome.