We found that p16Ink4a-negative cancer nests were more infiltrated by effectors of adaptive immune response (CD8+, CD4+ T lymphocytes) and demonstrated higher cytotoxic activity of immune cells (GZB+) while p16Ink4a status has no impact on number of innate effectors (CD56+) and regulatory (FOXP3+, CD68+) infiltrates. This evidence concerns the gene CD68 and cancer.