It is known that in response to infection, Toll-like receptors (TLR) bind to bacterial-derived lipopolysaccharide (LPS) and trigger an inflammatory response by activating the nuclear factor-kB (NF-kB) signaling pathway, which leads to the secretion of inflammatory cytokines, both pro-inflammatory and anti-inflammatory, further boosting hematopoiesis, phagocytosis, and leukocyte recruitment24. The gene discussed is NFKB1; the disease is infection.