Interestingly, while the inferred increases of lipopolysaccharide (a(CHEBI:lipopolysaccharide)) bacterial infection (path(SDIS:“bacterial infection”)) seem biologically implausible to occur during the 5 hour TNF treatment used to generate the data set, these mechanisms are aligned with reports that LPS and TNF activate very similar transcriptional responses in endothelial cells [39]. The gene discussed is TNF; the disease is bacterial infectious disease.