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]. The gene discussed is C5AR2; the disease is Sepsis.