Site directed mutagenesis of the predominant CaMKII phosphorylation site of RyR2 to mimic constitutively phosphorylated (RyR2-S2815D) and dephosphorylated (S2815A) channels, showed that CaMKII-dependent phosphorylation of RyR2 increases channel open probability and the risk of heart failure in mice following transverse aortic constriction [6], [7]. Here, CAMK2G is linked to heart failure.