TNFRSF1A and bacterial infectious disease: 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.