Previous studies have suggested an important role for the inward rectifier K⁺ current (I_K1) in stabilizing rotors responsible for ventricular tachycardia (VT) and fibrillation (VF). To test this hypothesis, we used a line of transgenic (TG) mice overexpressing Kir 2.1-GFP fusion protein in a cardiac-specific manner. Optical mapping of the epicardial surface in ventricles showed that the Langendorff-perfused TG hearts were able to sustain stable VT/VF for 350±1181 seconds at very high dominant frequencies (DF) of 44.6±4.3 Hz. In contrast, tachyarrhythmias in wild-type (WT) hearts were short-lived (3±9 seconds), and the DF was 26.3±5.2 Hz. The stable, high frequency, reentrant activity in TG mice slowed down, and eventually terminated in the presence of 10 µM Ba²⁺, suggesting an important role for I_K1. Moreover, by increasing I_K1 density in a two-dimensional computer model having realistic mouse ionic/action potential properties, a highly stable, fast rotor (45 Hz) could be induced. Simulations suggested that the TG hearts allowed such a fast and stable rotor due to both greater outward conductance at the core and shortened action potential duration in the core vicinity, as well as increased excitability, in part due to faster recovery of Na⁺ current. The latter resulted in a larger rate of increase in the local conduction velocity as a function of the distance from the core in TG compared to WT hearts, in both simulations and experiments. Finally, simulations showed that rotor frequencies were more sensitive to changes (doubling) in I_K1, compared to other K⁺ currents. In combination, these results provide the first direct evidence that I_K1 upregulation in the mouse heart is a substrate for stable and very fast rotors.