N-cadherin is a calcium-dependent glycoprotein that mediates intercellular adhesion; its deletion resulted in dilated cardiomyopathy; slow conduction and higher conduction anisotropy and then ventricular tachycardia in a mouse model; loss of T-tubules (crucial for synchronization of myofilament contraction), suggesting that surface structure alterations are an integral part of the remodeling process during cardiac failure; and altered gap junction (due to down- and mis-regulation of channels) which leads to conduction block and reentrant arrhythmias [43]. This evidence concerns the gene CDH2 and heart failure.