During sepsis, however, the endothelium becomes activated either directly by pathogen-associated molecular patterns (PAMPs) from bacteria, viruses, and fungi or indirectly through neutrophil extracellular traps (NETs) and proinflammatory cytokines like tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 (IL-1) (4). This evidence concerns the gene IL6 and Sepsis.