Among critically ill patients, sepsis is a leading cause of death in the early disease course as a result of a dysregulated proinflammatory phase (systemic inflammatory response syndrome [SIRS]) characterized by high levels of IL-1β, TNF-α, and monocytes expressed with human leukocyte antigen (HLA)-DR, or of a later predominating immunosuppressive recovery phase (compensatory anti-inflammatory response syndrome [CARS]) characterized by anti-inflammatory IL-10 and monocytes with reduced expression of HLA-DR [98,99]. This evidence concerns the gene IL10 and systemic inflammatory response syndrome.