Recently, we have found that cancer immune surveillance as represented by tumor infiltrating lymphocytes (TILs) and tumor associated macrophages (TAMs) depends on p16INK4a expression regardless to high-risk HPV-DNA status [5] as various immune effectors contribute to improved clinical outcomes in patients with p16-positive and p16INK4a-negative tumors. This evidence concerns the gene CDKN2A and neoplasm.