Compared with the wild-type channel, the mutant HERG/MiRP1 (V65M) channel detected in LQTS patients has a shorter current inactivation time, which may reduce the IKr current density of cardiomyocytes, weakening the cardiomyocytes' ability to repolarize sudden membrane depolarization (56). Here, KCNH2 is linked to familial long QT syndrome.