Furthermore, it is well established that pathogen-induced type I IFN results in ISG expression but also in IFNα and IFNβ secretion resulting in an autocrine amplification loop.45 This amplification loop seems to be activated upon infection with the ADP-heptose-deficient mutant, as blocking of the type I IFN receptor decreases IFN signaling as well as IFN-dependent target gene expression (Supplementary Figure S4). The gene discussed is IFNA2; the disease is infection.