If p53 indeed controls the crossroad between cancer and aging, then tampering with p53 activity could either yield longer lifespan, albeit at the cost of increased cancer risk, when its activity is diminished, or low tumor risk, at the cost of a shortened lifespan, if its activity is increased (Campisi, 2002; Donehower, 2005). The gene discussed is TP53; the disease is neoplasm.