In sepsis, activation of NF-κB is secondary to activation of TLR 2 and 4 by e.g., by wall fragments of Gram-negative (e.g., lipopolysaccharide; LPS) or Gram-positive bacteria (e.g., peptidoglycan; PepG) and/or pro-inflammatory cytokines including tumor-necrosis factor-α (TNF-α) or interleukin-1 (IL-1). The gene discussed is NFKB1; the disease is Sepsis.