Cell cycle arrest in senescence is mainly mediated via the following major tumor suppressor pathways: the p53/cyclin-dependent kinase inhibitor 1A (p21/WAF1/ CIP1) pathway and cyclin-dependent kinase inhibitor 2A (p16/INK4A)/ retinoblastoma protein (pRB) pathway, and can be induced by cellular stress, leading to DNA damage [6]. The gene discussed is CDKN1A; the disease is neoplasm.