Pathophysiologic mechanisms involved in such infections are a variety of bacterial virulence factor that this organism expresses [11]—binding of significant amounts of human serum albumin to a specific protein receptor on the cell wall of the organism, production of proteolytic enzymes by the bacteria, and expression of a surface protein, Protein L, which binds to the κ light-chain variable region of the human immunoglobulin molecule initiating the release of inflammatory mediators. The gene discussed is PROS1; the disease is infection.