Based on experimental data it is assumed that the infection leads via TLR or NOD1 signaling to an activation of host MAP-kinases (e.g., p44/42 and p38) as well as the NFκB pathway and subsequently to an induction of a pro-inflammatory immune response (Rasmussen et al., 1997; Hanada et al., 2003; Strober et al., 2006; Bastidas et al., 2013; Zhou et al., 2013). The gene discussed is NFKB1; the disease is infection.