In clinical practice, anti-CTLA-4 monoclonal antibody, an immune checkpoint inhibitor that not only blocks the CTLA-4 axis but also depletes Tregs, has been utilized as an effective cancer immunotherapy.5,6 However, CTLA-4 blockade systemically depletes Tregs and frequently causes serious autoimmune adverse events, resulting in treatment cessation and long-term use of immunosuppressive agents.7,8 To overcome these systemic side effects, therapeutic techniques that locally target Tregs are needed. The gene discussed is CTLA4; the disease is cancer.