Mechanistically, IGFBP-6 can be O-β-GlcNAc-modified at Ser204 during HBV/HCV infection, diminishing IGF-II binding and potentially increasing free IGF-II, which contextualizes how inflammatory/metabolic fluxes may tune IGFBP-6 function in chronic viral hepatitis [64]. Here, IGFBP6 is linked to animal viral hepatitis.