Though the exact pathobiology of ARDS, sepsis and septic shock is not clear, there is significant evidence to suggest that inflammation and disruption of the hemostatic system as a result of platelet-leucocyte interaction and consequent enhanced production of inflammatory cytokines such as interleukin (IL)-1β, IL-8, monocyte chemotactic protein 1 and tumour necrosis factor-alpha (TNF-α) play a major role [1–5]. The gene discussed is TNF; the disease is Sepsis.