RYR2 and heart failure: 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].