CDK4/6i–induced senescence is characterized by significant remodeling of the chromatin landscape, most notably the activation of genomic enhancers that drive transcriptional programs including luminal differentiation, the senescence-associated secretory phenotype (SASP), apoptotic evasion, and tumor cell immunogenicity–all phenotypic features of tumor cells responding to CDK4/6 inhibition (25, 30). This evidence concerns the gene CDK4 and neoplasm.