TRIM11 is an E3 ubiquitin-protein ligase that functions as a multifaceted cellular regulator with roles in neurodegeneration, innate immunity, and metabolism. As an E3 ligase, TRIM11 promotes proteasomal degradation of target proteins including tau, PAX6, and AIM2 1. In Alzheimer's disease, TRIM11 is markedly downregulated in affected brains, and restoration of TRIM11 expression protects against tau aggregation through multiple mechanisms: promoting degradation of mutant and normal tau, acting as a molecular chaperone to prevent tau misfolding, and dissolving preformed tau fibrils 1. In cardiac ischemia-reperfusion injury, TRIM11 mediates Nap1L1 ubiquitination and degradation to restore antioxidant gene expression via the Lrp6/Trim11/Nap1L1 axis 2. Regarding immune regulation, TRIM11 negatively regulates regulatory T cell differentiation by promoting AIM2 autophagic degradation, thereby promoting autoimmune responses 3. In lymphomas, TRIM11 elevation promotes cell proliferation by activating β-catenin signaling through Axin1 ubiquitination degradation 4. Additionally, TRIM11 modulates glycolytic flux and insulin signaling through regulation of glucose transporters 5. These diverse functions position TRIM11 as a potential therapeutic target for neurodegenerative diseases, autoimmunity, and cancer.