On the one hand, CaMKII expression and activity increases were observed in various species with atrial tachycardia and fibrillation, such as human with chronic AF (Neef et al., 2010; Voigt et al., 2012), goat with long-standing AF (Greiser et al., 2009) and canine with pacing-induced atrial tachycardia remodeling (Wakili et al., 2010), showing the role of AF in promoting CaMKII overexpression and hyperactivities. This evidence concerns the gene CAMK2G and atrial tachycardia.