Consistent with p16 being a major player in cellular senescence, genetic ablation of p16-positive cells, using the INK-ATTAC (Baker et al., 2011) and p16-3MR mice (Demaria et al., 2014), reduced senescent cell burden and improved healthspan, both in a progeria model, as well as naturally aged WT animals. This evidence concerns the gene CDKN2A and progeroid syndrome.