Viral hepatitis provides a clear example of post-translational control: O-β-GlcNAc modification of IGFBP-6 at Ser204 reduces IGF-II binding, implying that inflammatory and metabolic fluxes through the hexosamine pathway can shift IGFBP-6’s capacity to sequester IGF-II in infected livers [64]. Here, IGF2 is linked to animal viral hepatitis.