Furthermore, Tye et al. (132) have proposed a novel role for TLR2 in promoting gastric tumorigenesis independent of inflammation, whereby up-regulation of TLR2 within epithelial tumor cells, rather than infiltrating inflammatory cells, by the uncontrolled activation of the oncogenic transcription factor STAT3, promoted gastric tumor cell proliferation, and survival via up-regulation of anti-apoptotic genes [e.g., BCL2-related protein A1 (BCL2A1), baculoviral IAP repeat containing 3 (BIRC3), and B-cell CLL/lymphoma 3 (BCL3)]. This evidence concerns the gene BCL3 and neoplasm.