Of the 130 million attendances to emergency departments (EDs) in the United States each year, ≈7 million (6%) are a result of acute chest pain.1 The assessment and triage of such patients has become increasingly complex because now only a small proportion of those with acute myocardial infarction (AMI) have the diagnostic ECG change of ST-segment elevation.2 Consequently, the identification of patients with AMI has become almost totally dependent on the measurement in the systemic circulation of cardiac troponin (cTn) I or cTnT. The gene discussed is TNNT2; the disease is myocardial infarction.