CD86 and neoplasm: Moreover, genome-wide analyses of melanoma models revealed that H3K4me3 was increased on DC maturation genes such as CCR7 and CD86 [204], while De Beck, L., et al. [205] fund that a dual inhibitor of histone methyltransferase G9a and DNMTs could jointly increase the therapeutic efficacy of DC vaccination by arresting tumor cell cycle and delaying tumor growth of tumor-bearing mice, indicating the critical role of the cellular epigenetic regulation in modulating DC phenotypes, maturation and antitumor responses.