This dual effect highlights the therapeutic potential of targeting the CoREST-NOLC1 axis: inhibiting this pathway both blocks a pro-tumor mechanism and generates tumor-specific antigens that may sensitize “immune-cold” cancers to immunotherapies like checkpoint blockade, warranting follow-up in vivo studies to evaluate the role of the CoREST complex in regulating RNA splicing and shaping tumor immunogenicity. This evidence concerns the gene NOLC1 and cancer.