Suggested underlying mechanisms of tumor progression were (1) the limited infiltration of CD8+ T cells; (2) the enhanced infiltration of neutrophils in the TME, as P. gingivalis upregulates the expression of chemokines, such as CXCL1, CXCL2 and CXCR2, well known as neutrophil chemoattractants; and (3) the P. gingivalis-mediated modulation of the infiltrated neutrophil function, through induction of the production of neutrophil-derived elastase, a fundamental component of neutrophil extracellular traps (NETs) that exacerbate tumor growth [62]. The gene discussed is CXCL2; the disease is neoplasm.