Both p16 and p53 are major intermediates in cell senescence, a powerful tumour suppressor mechanism in the form of a permanent proliferative arrest that occurs after extensive normal cell proliferation and telomere shortening, or after oncogene activation or other stresses (Chandler and Peters, 2013; Gorgoulis et al., 2019; Wang et al., 2022). Here, CDKN2A is linked to neoplasm.