This was attributed to the recruitment of CCR6+ Treg cells by P. gingivalis through tumor cells, thereby reducing the proportion of effector CD8+ T cells in tumor-infiltrating lymphocytes and inhibiting their effector function, which in turn formed an immunosuppressive microenvironment in the TME and promoted the development of the malignant phenotype of OSCC (53). This evidence concerns the gene CD8A and neoplasm.