Thus, the shedding of F11R-containing microparticles from platelets and endothelial cell membranes, and the action of proteases degrading the protein in intercellular junctions of EC that disappear during inflammatory processes, and/or on the surface of the plasma membrane of platelets, may all represent alternate mechanisms operating during inflammatory processes that are responsible for the appearance of soluble and microparticle-bound F11R molecules in the plasma and serum of patients with cardiovascular diseases. The gene discussed is F11R; the disease is cardiovascular disorder.