Our data demonstrate not only a link between p53 and MCP-1 activation, but also suggests that functional p53 inactivation, either via E6-mediated degradation in the context of HPV-induced carcinogenesis [31] or after p53 mutation in other forms of human cancer [32], could affect immunological surveillance by abrogating intercellular communication between somatic cells and cell of the monocyte/macrophage lineage. Here, CCL2 is linked to cancer.