In the mutant tissue, it took a shorter period of time for multiple rotors to form and co-exist, suggesting that the T634S-hERG mutation effectively destablized the re-entrant excitation, leading to an increased maximum number of co-existing rotors (from 12 rotors in the WT case to 15 rotors in both mutant cases), suggesting an increased degree of un-coordinated ventricular excitation, a main feature of cardiac arrhythmias. This evidence concerns the gene KCNH2 and cardiac rhythm disease.