We showed that resminostat suppressed expression of IFIT-1 in HepG2, Hep3B, and PLC/PRF/5 cells after exogenous IFN-β stimulation, possibly preventing the induction of an antiviral state within hepatoma cells, thereby constituting a possible positive modulator for oncolytic virotherapy in tumor cells exhibiting a residual intact antiviral IFN response (see Supplementary Figure S2). The gene discussed is IFIT1; the disease is neoplasm.