The overexpression of COX-2 has been reported due to multiple stimuli, including in response to oncogenes (like HER-2/neu); tumor simulator molecules such as ceramides, vasoactive peptides, bile acids, phorbol esters, endothelin-1, and methanandamide; growth factors (like EGF); pro-inflammatory cytokines such as TNF-α, IL-1β, NF-IL6, NF-κB, and AP-1; bacterial lipopolysaccharide; nuclear factor of activated T cells (NFAT); and viral infection (polyomavirus enhancer activator-3 (PEA3)). Here, TNF is linked to neoplasm.