For EPEC, the combined effects of NleE and NleC appear to allow the pathogen to exert exquisite control of NF-κB signalling stimulated by both TLR and death receptor signalling, and despite the fact that inflammation ultimately results from infection with EPEC, these effectors may allow the pathogen to delay innate immune responses long enough to establish infection and disseminate to other hosts (Wickham et al., 2007b). This evidence concerns the gene NFKB1 and infection.