TNNI3 and cardiac hypertrophy: The development of an HCM phenotype with cardiac hypertrophy, fibrosis, and the activation of the fetal gene program in both +/+ and +/− R21C mice supports a negative-dominant effect of this pathogenic mutant to the wt cTnI that is intensified to diastolic dysfunction and excitation-contraction uncoupling upon long-term ablation of cTnI phosphorylation (Dweck et al., 2014).