TP53 and neoplasm: For example, although transient cell senescence, which is indicative of functional p53 signaling in response to many forms of DNA damage, is recognized as a tumor suppressor mechanism, persistent senescence accompanied by p53 inactivation would promote a senescence-associated secretory phenotype (SASP), which stimulates the secretion of numerous proinflammatory cytokines and growth factors that may modulate the epigenome and disrupt normal tissue structure and function [20].