CXCL10 and neoplasm: Consistently, in preclinical models of ovarian cancer and melanoma, epigenetic reprogramming due to EZH2 knock down or pharmacological inhibition enhanced the expression of Th1-recruiting chemokines (e.g., CXCL9, CXCL10), increased tumor-infiltrated CD8+ T cells, and improved the efficacy of ICB-based immunotherapy [106,107].