The latter is supported by: (a) our recent study in DMD induced pluripotent stem cell–derived cardiomyocytes (iPSC‐CMs) demonstrating prominent arrhythmias in the form of delayed afterdepolarizations (DADs) known to result from Ca2+‐overload16; (b) studies in mdx mice cardiomyocytes showing ‘leaky’ Ryanodine receptor (RyR) and abnormal Ca2+ handling.17, 18, 19. This evidence concerns the gene RYR2 and Duchenne muscular dystrophy.