Numerous studies report that after the binding of TLR5 to the specific ligand, it induces the myeloid differentiation gene 88 (MYD88), which triggers activation of the tumor downstream signaling pathways including NF-κB, mitogen-associated protein kinase (MAPK), and interferon regulatory factors (IRFs) [119]. The gene discussed is NFKB1; the disease is neoplasm.