Recently, loss-of function mutations in KCND3 (potassium voltage-gated channel, Shal-related subfamily, member 3) have been identified causing SCA19/22 [4, 5], whereas gain-of function mutations in KCND3 were implicated in Brugada syndrome and atrial fibrillation [6–8]. Here, KCND3 is linked to Brugada syndrome.