Although anti-PD1 immunotherapy is sufficient to recruit CD8+ T cells into the tumor microenvironment, it is not sufficient to kill BMI-1+ CSCs.193 Inhibition of BMI-1 de-represses H2AK119ub-decorated target genes and increases DNA-damage, stimulating the inflammatory response and CD8+ T cells recruitment.193 In summary, joint targeting of immune checkpoints and PcG proteins appears to be a new promising therapeutic approach to efficiently counter cancer progression by stimulating the immune response.191–193. This evidence concerns the gene CD8A and cancer.