Initially, the proinflammatory response was believed to be the major cause of mortality in patients with sepsis and was frequently targeted for therapeutic intervention.5 However, efforts to improve outcomes by targeting proinflammatory cytokines and mediators, such as TNF and IL‐1β antagonists, endotoxin antagonists, Toll‐like receptor (TLR) blockers, and platelet activating factor inhibitors, have been unsuccessful.6 The gene discussed is TNF; the disease is Sepsis.