Taken together, the activation of the cellular senescence mechanism following a DNA damage response was associated with aging, and it could induce the critical signaling pathways of TP53 and Retinoblastoma 1 (RB), the major tumor-suppressor genes, suggesting that the DNA damage response is a common mediator of cellular senescence and, further, that genomic instability plays a causative role in the aging process [63]. The gene discussed is TP53; the disease is neoplasm.