It has been demonstrated that EZH2 promotes tumor development through a cell-extrinsic mechanism involving inhibition of the antitumor activity of NK cells, the major components of the innate immune response, which are generally recruited to tumor sites with chemokines, such as CXCL9, CXCL10 and CXCL11, to explicate their immune function [22,54]. The gene discussed is CXCL10; the disease is neoplasm.