Although pharmacological therapeutic approaches developed over the past 50 years have considerably improved quality of life for patients with heart disease, these common pharmacological interventions (β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor II-antagonists, and diuretics) do not interact with or demonstrably curtail the relevant underlying intracellular signal transduction mechanisms that cause or intensify the development and progression of heart disease [1, 2]. This evidence concerns the gene ACE and heart disorder.