The first in vivo studies establishing CaMKII as a potential target for cardiac arrhythmias and structural heart disease were conducted by the use of a pharmacological inhibitor such as KN-62 or KN-93 and a CaMKII inhibitory peptide (Zhang et al., 2005; Vila-Petroff et al., 2007; Liu et al., 2011). This evidence concerns the gene CAMK2G and cardiac rhythm disease.