It was demonstrated that the combination of 3-Deazaneplanocin A (HMT inhibitor) and Vorinostat (HDAC inhibitor) had synergistic effect on non-small-cell lung carcinoma cells, which might be explained by the fact that HDAC activity is required for histone methyltransferase EZH2 caused transcriptional repression (EZH2 interacts with HDACs through PRC2 protein EED) [23]. The gene discussed is HDAC9; the disease is non-small cell lung carcinoma.