In sepsis, the endothelium is activated directly by pathogen-associated molecular patterns (PAMPs) of bacteria, viruses, and fungi or indirectly via neutrophil extracellular traps (NETs) and proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 (IL-1) (Figure 1A) (24–27). Here, TNF is linked to Sepsis.