Given that CaMKII can act as a proarrhythmic, feed-forward, signal in heart45, it is possible that arrhythmia and reduced cardiac function might contribute to the increased total CaMKII level in cKO mice, which might be underlying the discrepancy of total CaMKII levels in PRMT1-depleted cardiomyocytes. This evidence concerns the gene PRMT1 and Arrhythmia.