CTLA4 is an inhibitory immune checkpoint receptor that functions as a major negative regulator of T cell responses 1. It acts as a decoy receptor with substantially higher affinity for B7 family ligands (CD80 and CD86) compared to the stimulatory coreceptor CD28, allowing it to competitively suppress T cell activation 12. This inhibitory function is critical for maintaining immune homeostasis; dysregulation of CTLA4 is implicated in both autoimmunity and cancer. In cancer immunotherapy, CTLA4-blocking monoclonal antibodies (ipilimumab, tremelimumab) enhance anti-tumor T cell responses and are approved for melanoma, non-small-cell lung cancer, and renal cell carcinoma 34. Conversely, in autoimmune diseases including systemic lupus erythematosus, type 1 diabetes, and celiac disease, CTLA4 genetic variants are associated with disease susceptibility, suggesting insufficient inhibitory signaling contributes to pathogenesis 5. CTLA4 polymorphisms affecting receptor structure and function have been identified as disease-associated variants 6. Furthermore, CTLA4-CD28 fusion mutations in T cell lymphomas convert inhibitory to activating signals, promoting malignant T cell proliferation 7. Thus, CTLA4 represents a critical immune checkpoint with therapeutic relevance in both enhancing anti-tumor immunity and restraining autoimmune responses.