Analysis of CMs differentiated from the same iPSC line, carrying the DSG2-G638R mutation, showed that the expression of NDPK-B was elevated, via activating SK4 channels, contributing to arrhythmogenesis, and, hence, NDPK-B has been proposed as a potential therapeutic target for treating arrhythmias in patients with ACM [84]. This evidence concerns the gene NME2 and Arrhythmia.