Interestingly, different p16INK4A-positive cell elimination mouse models showed diverse phenotypes with the p16INK4A-INK-ATTAC model delaying aging phenotypes and increasing lifespan [72], while in the p16INK4A-3MR model wound healing was disturbed [41], and in p16INK4ACre;DTA mice liver fibrosis and reduced health-span were observed [39]. This evidence concerns the gene CDKN2A and Hepatic fibrosis.