Cardiac transient outward currents with fast recovery kinetics (Ito,f ) and somatodendritic A-type currents (ISA ) are mediated by Kv4 channels. Reverse-biased opening is thought to underlie cumulative inactivation of Kv4 channels during prolonged depolarizations like heart action potentials or dendritic plateau potentials. Thus, a modulation of Kv4 channel deactivation affects macroscopic inactivation. Here, we correlated inactivation and deactivation kinetics of Kv4.2 channel complexes. Kv4.2 was coexpressed with Kv Channel Interacting Proteins (KChIPs) and dipeptidylaminopeptidase-like proteins (DPPs) in HEK 293 cells. A-type currents and deactivation tail currents were recorded under whole-cell voltage-clamp. Our data suggest that the Kv4.2 N-type inactivation domain is not necessary for active modulation of current kinetics by accessory subunits. In Kv4.2[Delta]2–10 channels tail currents, cumulative inactivation and recovery from inactivation were all accelerated by KChIP2 and DPPX in an additive manner. Ternary complexes containing both KChIP2 and DPPX deactivated on a submillisecond time scale. Cumulative inactivation and recovery from inactivation were complete in less than 100 ms. Rapid kinetics let Kv4.2 channel complexes act like a transient switch with minimal refractoriness. Supported by the Deutsche Forschungsgemsinschaft (Ba2055/1-1,2; Ba2055/1-3)