Lin et al. [25] observed a potential role for CaMKII in atrial structural remodeling (Ryanodine receptor-mediated calcium leak drives progressive development of an AF substrate in a transgenic mouse model) as demonstrated in a transgenic mouse model with increased sarcoplasmic reticulum diastolic calcium leak, atrial dilation, and decreased electrical conduction, leading to increased AF susceptibility [26]. Here, CAMK2G is linked to atrial fibrillation.