Well-known tumour suppressor genes such as TP53 and CDKN2A, encoding p53 and p16, similarly affect cell cycle checkpoint, apoptotic and repair pathways; absence of the wild-type p53 or p16 proteins has effects on cell cycle kinetics, response to DNA damage and apoptosis, but these proteins are not necessarily good targets for treatment, except through gene therapy, necessitating identification of effectors of tumour suppressor signalling pathways, to define new therapeutic targets. Here, CDKN2A is linked to neoplasm.