EZH2 and neoplasm: Mechanistically, EZH2 methyltransferase activity was directly responsible for suppressing many SASP-related chemokine and cytokine genes, such that genetic or pharmacological inhibition of EZH2 in tumor cells triggered to senescence following T/P therapy led to a marked reduction in H3K37me3 levels at these loci and a phenotypic switch from a pro-angiogenic to a pro-inflammatory SASP program.