Following the removal of IκBs, the released NF-κB complexes are free to enter the nucleus [4], where they bind to distinctive decameric DNA elements, known as κB sites, and regulate transcription of a diverse array of genes, encoding numerous inflammatory mediators, immunoregulators, apoptosis inhibitors, developmental factors and other genes responsible for moulding the host defence responses to stress, injury and infection [4,5]. Here, NFKB1 is linked to infection.