Background: Sudden cardiac death in heart failure patients occurs predominately in the morning hours. Delayed ventricular repolarization, measured as prolonged QT interval on the ECG, heralds increased susceptibility to sudden cardiac death. Potassium Channel Interacting Protein 2 (KChIP2) is a subunit of the K+ channel Kv4.3 responsible for conducting the fast transient outward current, (Ito,f) and important for ventricular repolarization. KChIP2 is suggested to be responsible for the circadian rhythm in repolarization duration, ventricular arrhythmias and sudden cardiac death. Objective: We made the hypothesis that there is no circadian rhythm in QT interval in the absence of KChIP2. Methods: Implanted telemetric devices recorded ECG continuously for 5 days in conscious male C57BL6 wild-type mice (WT, n=9) and KChIP2-/- mice (n=9) in light:dark periods and in complete darkness. QT intervals were determined from all RR intervals and corrected for heart rate (QT100= QT/(RR/100)1/2). Moreover, QT intervals were determined from complexes within the RR range of mean-RR±1% in the individual mouse (QTmean-RR). We generated individual, cosine fits to hourly data points and thereby obtained the rhythm parameters mesor (average), amplitude and phase. Period was set to 24 hours. Results: RR intervals are 125±5 ms in WT and 123±4 ms in KChIP2-/- (p=0.81), and QT intervals are 52±1 and 52±1 ms, respectively (p=0.89). No ventricular arrhythmias or sudden cardiac deaths were observed. We find similar diurnal (light:dark) and circadian (darkness) rhythms of RR intervals in WT and KChIP2-/- mice with the amplitudes of the circadian rhythms being 14.1±2.3 and 14.2±1.9 ms, respectively (p=0.96; Figure panel A). Circadian rhythms in QT100 intervals are present in both groups, but at small amplitudes: 1.6±0.2 and 1.0±0.3 ms in WT and KChIP2-/-, respectively (p=0.15; Figure panel B). A diurnal rhythm in QT100 intervals was only found in WT mice. On the other hand, QTmean-RR intervals in both groups display clear diurnal and circadian rhythm, where the amplitude of the latter is 4.0±0.3 and 3.1±0.5 ms in WT and KChIP2-/-, respectively (p=0.16; Figure panel C). Conclusion: In the present study, we falsify our hypothesis and conclude in contrast to previous findings that KChIP2 expression cannot underlie the circadian rhythm in repolarization, because mice deficient of KChIP2 have a preserved circadian rhythm in QT interval. The molecular link governing circadian rhythm in sudden cardiac death remains therefore unknown.