Despite these limitations, a few studies indicated that the mechanisms promoting increased tumourigenesis in OSCC in the case of P. gingivalis/F. nucleatum coexistence are the activation of key molecules for tumour mass growth and unrestricted proliferation of oral epithelial cells, such as cyclin D1, and proangiogenic and pro-inflammatory cytokines such as IL-6 and IL-8, TNF-α, IL-18, apoptosis-associated granule protein containing CARD (ASC), MMP-9, and caspase-1. The gene discussed is TNF; the disease is neoplasm.