Activation of tumour suppressor pathways and upregulation of cyclin-dependent kinase inhibitors p16INK4a (encoded by CDKN2A) and p21CIP1 (CDKN1A) lead to permanent cell cycle arrest, induction of survival genes, and production of a bioactive secretome, referred to as the senescence-associated secretory phenotype (SASP). Here, CDKN1A is linked to neoplasm.