Through HDL- or LDL-mediated interaction with apolipoprotein A-I (Apo-A1), TTR significantly affects cholesterol efflux leading to amyloid deposition and cytotoxicity.[101,103] These structural changes in TTR result in extracellular protein deposition in cardiac tissues and coronary arteries ultimately altering TTR level and its functioning during CAD. The gene discussed is TTR; the disease is coronary artery disorder.