CDKN2A and cancer: Contrary to the assumption that senescence and tumorigenicity are always permanently connected and mutually exclusive, recent data monitoring one of the well-established markers of senescence, p16INK4a, in mice indicates that the activation of this hallmark of cellular senescence is, in fact, a characteristic of all emerging cancers [197], thus suggesting that cellular senescence is a quasi-stable and/or plastic cellular state prone to oncogenesis rather than a cancer preventive mechanism.