Though, our study does not rule out crosstalk independent engagement of the Nfkb2 pathway in activating RelB:p52 dimer in the hematopoietic compartment at a later stage of infection, epithelial RelA NF-κB activation defects coupled to aggravated early colon pathology and early onset of mortality in Nfkb2−/− mice suggested that the stromal requirement of Nfkb2, at least in part, lies within the intestinal epithelial cells in the initial events controlling early innate immunity and involves crosstalk regulation of RelA NF-κB activity (Figure 7I, also discussed later). This evidence concerns the gene NFKB1 and infection.