However, IFNβ affects the immune system via multiple mechanisms, such that it has been concluded that “IFN-1 are neither “good” nor “bad” regulators of inflammation, but that their protective or adverse character varies with more or less pronounce inflammatory environments.” (35) This may explain somewhat conflicting data in the literature regarding the role of interferons in mediating the response to endotoxemia and/or sepsis. The gene discussed is IFNB1; the disease is serum lipopolysaccharide activity.