HUMAN C-reactive protein (CRP) was originally observed in the plasma of patients with acute infections and was found to react with the C-polysaccharide of the pneumococcus.1 It is an acute-phase reactant, because of the pronounced rise in concentration after tissue injury or inflammation. This diagnostically sensitive but nonspecific marker for inflammation is produced primarily by the liver but also by lymphocytes.2 C-reactive protein appears to recognize both foreign pathogens and damaged host cells and can initiate their elimination by interacting with humoral and cellular effector systems in the blood.3 The work of Ross and others has clearly shown that arteriosclerosis involves a chronic inflammatory process.4 Thus, it is not surprising that a series of studies have now found a significant positive relationship between CRP concentration and coronary artery disease (CAD),5,6 although it remains unclear that this relationship is independent of other inflammatory markers.7 Hence, a 70-year-old test used to detect acute inflammation has now become a potential important marker for CAD. This commentary raises questions associated with the use of CRP as a screening device for CAD in asymptomatic patients.