Our results demonstrated that ectopic expression of EZH2 increased the viability (Fig. 2B, C, S3A-C) and proliferation (Fig. 2D, E, S3D and E) of HCC cells after Roblitinib treatment, leading to the antagonism, while under the same conditions, knockdown of EZH2 reduced cell viability (Fig. 2B, C, S3A-C) and proliferation (Fig. 2D, E, S3D and E), suggesting that knockdown of EZH2 may sensitize HCC cells to Roblitinib. The gene discussed is EZH2; the disease is hepatocellular carcinoma.