In both experimental (polymicrobial) sepsis and human sepsis/septic shock there is evidence for robust activation of the complement system, resulting in release of extremely strong proinflammatory products such as C5a, an anaphylatoxin that reacts with its receptors (C5aR, C5L2) on phagocytes (neutrophils, macrophages) and on a variety of organs to trigger numerous biological responses (enzyme release, chemotaxis, respiratory burst resulting in production of O2• and H2O2, and other responses) [1]. This evidence concerns the gene C5 and Sepsis.