The Pseudomonas lipid A moiety, for instance, is part of the Gram-negative bacterial cell wall constituent lipopeptide and able to activate NFκB in a Toll-like receptor (TLR)−4 dependent fashion (45), which subsequently leads to recruitment of innate immune cells to the infection site, further perpetuating host immune responses in order to combat the (opportunistic) pathogenic challenge (1). This evidence concerns the gene NFKB1 and infection.