In our study, we took advantage of two RyR2 knock-in mutants at S2814 which mimic unphosphorylated (S2814A) [7] and constitutively hyperphosphorylated (S2814D) [6] RyR2; the latter of which mimics high S2814 phosphorylation seen in multiple cardiac diseases including atrial fibrillation and heart failure [3,4,5]. The gene discussed is RYR2; the disease is heart failure.