Ryr2ADA/ADA mice have three substituted amino acid residues in the calmodulin (CaM) binding domain of RyR2 (RyR2-W3587A/L3591D/F3603A, RyR2ADA) that disrupt its CaM inhibition at diastolic and systolic Ca2+ concentrations and result in cardiac hypertrophy and the early death of RyR2ADA/ADA mice [15]. This evidence concerns the gene RYR2 and cardiac hypertrophy.