Targeted elimination of p16Ink4a-positive senescent cells in transgenic mice verified their contribution to age-related pathologies and dysfunctions.34,35 The causal role of senescent chondrocytes in posttraumatic OA pathogenesis has also been addressed using a similar strategy.16 The prosenescence role of Akt has been suggested in cancer cells and aging Caenorhabditis elegans. The gene discussed is CDKN2A; the disease is cancer.