Many anti-TB drugs are associated with a significant QT-interval prolongation caused by the inhibition of the human ether-a-go-go-related gene (hERG) potassium channel.4–10 This delays repolarization, resulting in a prolonged QT interval and increasing the risk of developing a potentially life-threatening ventricular arrhythmia known as torsades de pointes (TdP).11 It is therefore essential to evaluate the effects of novel and repurposed drugs on the QT interval, especially when given in combination with other drugs. Here, KCNH2 is linked to torsades de pointes.