Circulating IL-6 prolongs the action potential duration by enhancing L-type Ca2+ current (ICa,L), which causes phase 2 early afterdepolarization.[17] Moreover, IL-6 inhibits the rapid component of the delayed rectifier K+ current (Ikr), prolonging the action potential duration and QT interval.[18] Although serum IL-6 levels were not measured, IL-6-mediated enhancement of ICa,L and inhibition of IKr are the most likely mechanisms for QT interval prolongation and morphological T-U wave variability in our patient, leading to TdP. This evidence concerns the gene IL6 and torsades de pointes.