For instance, gain-of-function genetic mutations in voltage-gated potassium channel subunits KCNH2,6KCNQ1,7 and KCNJ27 are known to cause SQTS; conversely, loss-of-function mutations in cardiac voltage-gated calcium channels including CACNA1C,8CACNB2B,8 and CACNA2D9 cause SQTS and have phenotypic overlap with Brugada syndrome.8,9. Here, CACNA1C is linked to Familial short QT syndrome.