Proper repolarization of cardiac action potentials relies on a number of different Kþ channels. The exact composition of Kþ channels varies between atria and ventricles and thus is a prerequisite for the observed morphologic differences between atrial and ventricular action potentials. There is interest from a pathophysiologic perspective in identifying atrial selective Kþ channels. The rationale for this interest is the possibility of using atrial selective inhibition of Kþ channels for treating atrial fibrillation in a manner that avoids ventricular adverse effects. With these considerations in mind, substantial efforts have been devoted toward identifying atrial selective Kþ channels. For years the focus was on IKur current conducted by Kv1.5 channels and IKACh current conducted by Kir3.1/Kir3.4 channels. A newcomer to this field is a Ca2þ-activated Kþ channel with small conductance, known as the SK channel. Historically, the first evidence of cardiac SK channels reported in 1972 did not prompt additional investigations. These studies took advantage of the finding that the peptide toxin apamin could be isolated from bee venom. Apamin demonstrated ex vivo and in vivo effects in dogs and monkeys. Increased heart rate and force of contraction were observed with no obvious ECG effects or impact on blood pressure. Furthermore, apamin clearly was antiarrhythmic. Sporadic evidence of cardiac Ca2þ-activated Kþ channels and of rejection of their presence also was reported. Apamin later was demonstrated to be a selective target for SK channels, but evidence of cardiac SK channels was not reported until almost 30 years later. In 2003, evidence of human cardiac SK channels in addition to atrial selective expression with application of surprisingly low concentrations of apamin (50 pM) were reported. An atrial selective distribution had been suggested by other groups, but there also was abundant evidence, at least from an expression profile, that SK channels also were present in ventricles. From a functional perspective, there is an apparent atrial selective dominance of SK channel function. Whether this functional selectivity is a consequence of