Based on the finding that organism-wide TNFR1-deficiency has no differential response in the CLP model, and based on the knowledge that TNFR1 is essential in antimicrobial resistance, we tested the hypothesis that retention of TNFR1 on peritoneal WBC, but depletion of TNFR1 on potential TNF-target cells, responding to the inflammatory properties of TNF, may uncouple the beneficial from the harmful effects of TNF in sepsis, as predicted in recent opinion pieces (38). The gene discussed is TNF; the disease is Sepsis.