A study in Nature identifies an epigenetic mechanism in tumour cells that contributes to immune evasion. In two mouse models of ovarian cancer, combined inhibition of enzymes known to mediate epigenetic silencing in cancer — enhancer of zeste homologue 2 (EZH2) and DNA methyltransferases (DNMTs) — reduced tumour size, slowed tumour progression, and increased tumour T cell infiltration and T helper 1 (TH1)-type chemokine expression. By contrast, this inhibition did not reduce tumour size in immunodeficient mice, which suggests that epigenetic silencing of T cell-recruiting chemokines in cancer cells promotes tumour growth and progression. Furthermore, inhibition of epigenetic silencing significantly enhanced the in vivo efficacy of PD1 ligand 1 (PDL1) blockade and of adoptive T cell therapy. In human ovarian tumour tissue, high expression of EZH2 and DNMT1 significantly correlated with poor prognosis and a reduced number of tumour-infiltrating CD8+ T cells. Together, these data suggest that epigenetic silencing of chemokines in ovarian cancer reduces T cell recruitment to the tumour microenvironment and can thus shape the immune response. As immunotherapies require tumour infiltration of T cells, their efficacy could be augmented by epigenetic reprogramming in cancer patients, as shown here in mouse models.