Cancer cells can exit senescence through cell and non-cell autonomous mechanisms such as alterations within the tumor suppressor pathways p53-p21Cip1/Waf1 and pRB-p16INK4A or through the infiltration of immune cells, such as myeloid cells, that enable already arrested cells to escape from oncogene-induced senescence, and thus sustain tumor growth [19]. Here, CDKN2A is linked to neoplasm.