In several cancer models, including multiple myelomas and glioblastomas, the G9a inhibitor BIX01294 targeting G9a induces cell proliferation inhibition and autophagy-associated apoptosis by inactivating the mTOR/4EBP1 pathway and transcriptionally reducing c-MYC levels.213–215 A genome-wide study illustrated that the interaction between MYC and G9a, with the MYC MBII region as the binding point, affects MYC’s capacity to drive transcriptional repression and tumorigenesis. The gene discussed is MYC; the disease is glioblastoma.