NFKB1 and glioma: Conversely, tumors can exploit the activation of their TLRs to suppress apoptosis and promote proliferation via pathways such as NF-κB and MAPK.299 This has been corroborated in various types of tumors, including gliomas, hepatocellular carcinoma, lymphoma, and breast cancer.299–303 Additionally, these pathways facilitate the secretion of factors like IL-6, GM-CSF, and MMPs, promoting immune escape and a pro-tumoral niche.299,302,304,305 Inflammation induced by TLR-associated pathways also stands as one of the risk factors for various cancers.306