In the time since hERG was first identified as underlying the channels that mediate IKr [5, 6], loss-of-function hERG mutations have been found to be responsible for the LQT2 form of congenital long QT syndrome (LQTS), whilst the unique pharmacological promiscuity of the channel has been implicated in drug-induced LQTS [7]. This evidence concerns the gene KCNH2 and familial long QT syndrome.