The methylation of DLC1 protein induced by EZH2 is potentially reversible, which enables EZH2 inhibitors to increase the half-life of the DLC1 protein and, together with kinase inhibitors that can dephosphorylate and reactivate the tumor suppressor activity of DLC1 protein, to be used for treating tumors that express DLC1 mRNA but lack detectable levels of DLC1 protein. The gene discussed is DLC1; the disease is neoplasm.