Analysis of inflammatory ligand–receptor interactions revealed increased signaling through TGF-β, PDGF, and Antigen presentation and immune response and Adenosinergic signaling pathways (Figures 7B, D), while sepsis-induced enhanced interactions between Microglia 1 and Astrocytes 1 and 2 via PECAM1-CD38, and between Microglia 1 and Endothelial cells and Microglia 2 via PECAM1-PECAM1, suggesting increased neuroinflammation (55). This evidence concerns the gene TGFB1 and Sepsis.