These interactions activate the signaling cascade of NF-κB, resulting in the production of pro-inflammatory cytokines, i.e., interleukin 1β (IL1β), interleukin 6 (IL6), interleukin 8 (IL8/CXCL8), and tumor necrosis factor α (TNF-α), in addition to triggering the infiltration of polymorphonuclear cells (neutrophils, PMNs) to the site of infection [15]. The gene discussed is TNF; the disease is infection.