UACA (uveal autoantigen with coiled-coil domains and ankyrin repeats) is a multifunctional protein with roles in cell dynamics, apoptosis regulation, and inflammation. Structurally, UACA contains coiled-coil domains and ankyrin repeats 1, with widespread tissue expression including skeletal muscle, uveal tissues, and thyroid 12. Mechanistically, UACA modulates actin dynamics to regulate cell morphology and motility, with potential involvement in neurite formation. In apoptosis regulation, UACA induces Apaf-1 translocation from cytoplasm to nucleus, facilitating apoptosome activation 3. Conversely, UACA can mediate NF-κB-dependent antiapoptosis in cancer cells by blocking PAR-4 receptor GRP78 trafficking to the cell surface, enhancing apoptosis resistance 4. Additionally, UACA negatively regulates NF-κB signaling and inflammation, including roles in IκBα destabilization 5. Disease relevance spans autoimmune and malignant conditions. Anti-UACA autoantibodies are significantly elevated in panuveitis patients (19.6-28.1% vs. 0% in controls) 1 and Graves' disease (15% vs. 0%), particularly with ophthalmopathy (29-75% in severe cases) 2. In cancer, UACA upregulation associates with ICI therapy resistance in urothelial cancer 6, while downregulation occurs in non-small cell lung carcinoma, potentially reducing apoptotic thresholds 3. UACA expression correlates with breast cancer metastasis and poor prognosis 7, and participates in PANoptosis during acute liver failure 8.