Thus, we propose that NK cells do not mediate the inflammatory HBD + DIC phenotype in sepsis through IFN-γ but rather that persistent NK cell cytolytic dysfunction, stemming from a quantitative reduction in cell number and high levels of IL-6 [52, 54], translates into an impaired ability to induce apoptosis of activated macrophages [6]. The gene discussed is IL6; the disease is Sepsis.