Defects in Ca2+ handling are responsible for dysregulated Ca2+ homeostasis and cardiac arrhythmias, and occurrence of DADs is associated with intracellular Ca2+ overload.[37] We thus reasoned that Ca2+ handling abnormality engendered by TMEM43‐P386S is responsible for the arrhythmic phenotypes in ARVC. This evidence concerns the gene TMEM43 and arrhythmogenic right ventricular cardiomyopathy.