TNF can also trigger cell death by engaging TNF receptor I (TNFRI) along apoptotic or necroptotic pathways, which is believed to limit or exacerbate inflammatory responses, respectively.1 Excessive TNF release during fulminant bacterial infection can lead to a cytokine storm, vascular leakage driven by TNF-mediated endothelial damage, septic shock and death.2 The pro-death and inflammatory potential of TNF therefore need to be tightly regulated and cells have developed highly specialized means to control the biological outcome of TNFRI activation. Here, TNF is linked to bacterial infectious disease.