Strong preclinical data support the translatability of this approach to a clinical setting[115], including a recent report in which Ishiguro et al.[117] showed that the dual EZH2/G9a inhibitor GSK126 exerted a potent tumor-suppressive effect by activating an immune response through upregulation of interferon (IFN) signaling and by halting the IRF4-MYC axis. The gene discussed is EZH2; the disease is neoplasm.