Protein kinase A (PKA)-dependent phosphorylation of cardiac troponin I on Serine 23 and 24 residues was postulated to play a role in enhancing the rate of contraction and relaxation after beta adrenergic stimulation [23] and decreased phosphorylation of cardiac troponin I was observed in patients with heart failure [24], [25]. The gene discussed is TNNI3; the disease is heart failure.