Shaping of cardiac action potentials depends on a finely tuned orchestra of ion channels. Among them, K+ channels probably form the most diverse family. They are responsible for inwardly rectifying (I(Kl), I(KAch), I(KATP)), transient (I(to)), and sustained outward rectifying (I(Kur), I(Kr), I(Ks)) K+ currents. The properties of these cardiac K+ channels have recently been extensively reviewed. This article focuses on recent progress made toward understanding the molecular structure of the particular channel responsible for the slow outward K+ current I(Ks) and its implication in the delayed ventricular repolarization that characterizes the congenital long QT syndrome.