TAB3 (TGF-β-activated kinase 1 binding protein 3) is a regulatory component of the TAK1-TABs signaling complex with central roles in inflammatory and oncogenic pathways. As a binding partner of TAK1, a MAPKKK family member, TAB3 assembles into a complex activated by inflammatory stimuli including TNFα, IL-1β, and toll-like receptor ligands 1. TAB3 functions as a molecular adaptor that positively regulates canonical NF-κB and MAPK signaling cascades 1. Mechanistically, TAB3 promotes TAK1-STAT3 complex formation to activate downstream PIM1 expression in colorectal cancer 2, and interacts with GPX4 to modulate TAK1 kinase activity in nasopharyngeal carcinoma 3. TAB3 also negatively regulates autophagy through constitutive interaction with the autophagy mediator Beclin 1 4. Clinically, TAB3 expression is significantly elevated in multiple malignancies. High TAB3 levels correlate with poor prognosis in esophageal squamous cell carcinoma, associating with lymph node metastasis and reduced overall survival 5. TAB3 knockdown inhibits cancer cell proliferation and invasion through NF-κB pathway suppression 5. Conversely, TAB3 is required for viral replication; miR-532-5p exhibits antiviral activity against West Nile virus by suppressing TAB3 expression 6. In acute kidney injury, the METTL3/TAB3 axis drives renal inflammation, positioning TAB3 as a potential therapeutic target 7.