Indeed, selective removal of p16INK4a-positive senescent cells in p16-3MR transgenic mice has been shown to ameliorate multiple age-associated changes within the IVD tissue [31], while p16INK4a deletion has been reported to decrease ROS levels, the number of senescent cells and the SASP, as well as to rescue disc height index and ECM components’ expression levels in a mouse tail suspension-induced IDD model [32]. This evidence concerns the gene CDKN2A and intervertebral disk degenerative disorder.