In the ventricular cardiomyocytes of a myocardial infarction animal model, it was found that miR-223-3p levels were elevated, while expression of KCND2 and Ito were diminished resulting from the direct inhibition of KCND2 by miR-223-3p, and the upregulation of miR-223-3p promoted arrhythmia following myocardial infarction (94). This evidence concerns the gene KCND2 and Arrhythmia.