It is also well established that chronic CaMKII activity in cardiac disease is a major regulator of RyR2 function with arrhythmogenic consequences (Ai et al., 2005; Zhang et al., 2005; Terentyev et al., 2009; Belevych et al., 2012; Respress et al., 2012; Uchinoumi et al., 2016). This evidence concerns the gene CAMK2G and heart disorder.