Lipopolysaccharide, a putative ligand for TLR4, may promote tumour progression by acting directly on cancer cells, resulting in increased tumour cell–endothelial cell adhesion, tumour cell–extracellular matrix adhesion, and tumour cell–extracellular matrix invasion through NF-κB-mediated upregulation of β-1 integrin (Andrews et al, 2001; Wang et al, 2003). This evidence concerns the gene NFKB1 and neoplasm.