Considering the gain-of-function nature of KCNT1 mutations, potassium channel blockers, such as quinidine, may serve as a precision therapeutic option for KCNT1 mutation-associated SHE; however, conflicting reports exist on quinidine’s efficacy in treating SHE (66, 67), and its significant cardiac risks introduce substantial challenges. Here, KCNA3 is linked to sleep-related hypermotor epilepsy.