Considering that NDPK-B is an upstream regulator of SK4 channels, and both the SK4 blocker TRAM-34 and NDPK-B counter-actor PHP-1 reduced pacemaker activity and occurrence of arrhythmias in ARVC cells, we speculate that NDPK-B/SK4 upregulation might be a reason for arrhythmogenesis in ARVC. This evidence concerns the gene PLPPR4 and arrhythmogenic right ventricular cardiomyopathy.