Translocation of ISGF3 into the nucleus and subsequent binding to IFN-stimulated response elements (ISRE) drives the transcription of type I IFN and other IFN-stimulated genes (ISGs).44 The fact that type I IFN signaling is activated by both H. pylori wt and the ADP-heptose deficient ΔrfaE mutant, but more pronounced in the latter infection, is evident not only from the proteomics data (Figure 5(b)) but can also be shown by enhanced phosphorylation as well as protein expression of STAT1, STAT2 and IRF9 (Figure 5(d)). The gene discussed is STAT1; the disease is infection.