In addition to their regulatory roles in STAT1-mediated chemo-resistance, both DTX3L and ARTD9 could also be directly involved in editing or inhibiting the IFNγ-dependent host immune response against tumor cells through the termination of IFNγ-mediated gene expression and the inhibition of the extrinsic IFNγ-induced anti-proliferative and pro-apoptotic STAT1-IRF1-X-axis. The gene discussed is STAT1; the disease is neoplasm.