•  Previous studies have suggested that the K+ channel auxiliary subunit K+ channel‐interacting protein 2 (KChIP2) serves as a regulator of cardiac remodelling leading to heart failure and increased risk of arrhythmias. •  The results presented here show that the progression of cardiac remodelling and heart failure induced by transverse aortic constriction follows a similar time course in wild‐type and KChIP2−/− mice. •  Protein expression analysis shows that ventricular KChIP2 is significantly downregulated in heart failure in wild‐type mice. •  The electrophysiological analysis reveals enlarged J and T wave amplitudes and lower vulnerability to pacing‐induced ventricular arrhythmias in KChIP2−/− control mice compared to wild‐type control mice. Heart failure in wild‐type and KChIP2−/− mice prompted comparable prolongation of QT intervals and ventricular effective refractory periods. •  Collectively, these results demonstrate that KChIP2 does not influence the structural and functional development of heart failure. Moreover, in contrast to previously reported data, downregulation of KChIP2 expression in heart failure may reduce the risk of cardiac arrhythmia. Abstract  Abnormal ventricular repolarization in ion channelopathies and heart disease is a major cause of ventricular arrhythmias and sudden cardiac death. K+ channel‐interacting protein 2 (KChIP2) expression is significantly reduced in human heart failure (HF), contributing to a loss of the transient outward K+ current (Ito). We aim to investigate the possible significance of a changed KChIP2 expression on the development of HF and proarrhythmia. Transverse aortic constrictions (TAC) and sham operations were performed in wild‐type (WT) and KChIP2−/− mice. Echocardiography was performed before and every 2 weeks after the operation. Ten weeks post‐surgery, surface ECG was recorded and we paced the heart in vivo to induce arrhythmias. Afterwards, tissue from the left ventricle was used for immunoblotting. Time courses of HF development were comparable in TAC‐operated WT and KChIP2−/− mice. Ventricular protein expression of KChIP2 was reduced by 70% after 10 weeks TAC in WT mice. The amplitudes of the J and T waves were enlarged in KChIP2−/− control mice. Ventricular effective refractory period, RR, QRS and QT intervals were longer in mice with HF compared to sham‐operated mice of either genotype. Pacing‐induced ventricular tachycardia (VT) was observed in 5/10 sham‐operated WT mice compared with 2/10 HF WT mice with HF. Interestingly, and contrary to previously published data, sham‐operated KChIP2−/− mice were resistant to pacing‐induced VT resulting in only 1/10 inducible mice. KChIP2−/− with HF mice had similar low vulnerability to inducible VT (1/9). Our results suggest that although KChIP2 is downregulated in HF, it is not orchestrating the development of HF. Moreover, KChIP2 affects ventricular repolarization and lowers arrhythmia susceptibility. Hence, downregulation of KChIP2 expression in HF may be antiarrhythmic in mice via reduction of the fast transient outward K+ current.