Earlier work observed that the aging phenotype in progeria mice with a hypomorphic mutation in BubR1, a checkpoint gene, was partly restored by p16Ink4 deletion, but not by ablation of p19Arf, which results in inactivation of the p53/p21Cip1 pathway (34), and that genetic removal of p16-high cells has been established as an efficient form of potential senotherapy (35). Here, CDKN2A is linked to progeroid syndrome.