In the same study, the administration of an EZH2 inhibitor (CPI-1205) in bladder cancer and melanoma mouse models increased the cytotoxic activity of CD8+ effector T cells, altered the phenotype and function of Tregs, and increased susceptibility to ipilimumab, providing a rationale for combining immune checkpoint inhibitors and histone modification inhibitors against ICI-resistant cancers (Table 1). The gene discussed is CD8A; the disease is urinary bladder cancer.