All these discoveries suggest that investigation whether TMEM43 is involved in forming channels in cardiac and skeletal myocytes and whether mutation in TMEM43 directly affects function or distribution of various ion channels may open new avenues for developing targeted therapies for many TMEM43 mutation-induced devastating disorders, including ARVC and EDMD-related myopathies. This evidence concerns the gene TMEM43 and Arrhythmogenic right ventricular dysplasia.