Since N-cadherin anchors to a neighboring myocyte through its extracellular domain and is essential for cell–cell communication of cardiomyocytes in vivo and in vitro [9,24], ADAM10-dependent N-cadherin cleavage likely plays a vital role in non-ischemic cardiac diseases that are affected by the missing initial ectodomain cleavage, such as DOX-induced DCM. This evidence concerns the gene ADAM10 and familial dilated cardiomyopathy.