There, CrP synthesized in the liver upon interleukin-6 stimulation, represents a candidate mediator linking inflammation with occurrence of acute coronary syndromes.[8] In an animal model of atherosclerosis, CrP transgene expression accelerated aortic atherosclerosis,[9] whereas therapeutic inhibition of CrP improved outcome of experimental myocardial infarction.[10] Functional studies on neutrophils and human endothelial cells indicate that monomeric CrP, but not pentameric or native CrP, leads to neutrophil-granulocyte[11] and to endothelial-cell activation.[12]. The gene discussed is CRP; the disease is aortic atherosclerosis.