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C-reactive protein (CRP) is a protein whose baseline levels increase in response to acute or chronic inflammation. It is not only an inflammatory marker but also a well-established risk factor for cardiovascular disease. It is a common contributor to inflammation and thrombosis. In vivo, it is present in two distinct isoforms: a plasma form (pentameric CRP or pCRP) and a tissue form (monomeric CRP or mCRP). The latter, through its interaction with cellular elements of the inflammatory environment, is actively involved in the pathogenesis of arterial thrombosis in vivo. CRP’s interference with the hemostatic system is also observed in vitro. Indeed, owing to its binding affinity for phospholipids, CRP induces false phospholipid-dependent prolongations of coagulation times. The degree of coagulation time prolongation depends not only on the plasma CRP levels but also on the choice of reagent and automated testing system . Thus, high levels of CRP in a proven inflammatory context should alert biologists to possible analytical interference, which should be taken into consideration in the biological validation of both routine and specialized coagulation results.