IGFBP3 upregulation in uninfected cells treated with 5aza suggests that an inhibitor of IGFBP3 is normally methylated in AGS cells, and that 5aza demethylates the inhibitor to induce IGFBP3. EBV infection also strongly induces IGFBP3, but subsequent 5aza treatment does not further induce gene expression rather it partly reverses the effect of EBV on IGFBP3 induction. The gene discussed is IGFBP3; the disease is Epstein-Barr virus infection.