Reactive oxygen species of endogenous or exogenous origin induce and firm the senescent phenotype by a process that involves the response to DNA damage, epigenetic regulation and tumour suppression pathway activation (e.g. cell cycle control related proteins: p53 (cellular tumour antigen p53), p21 (p21Cip1, cyclin-dependent kinase inhibitor 1), pRB (retinoblastoma protein). The gene discussed is CDKN1A; the disease is neoplasm.