The Fc‐dSA3‐12 conjugate showed >100‐fold lower activity than TZ‐dSA3‐12 (Figure S4e, Supporting Information), and FcγR blockade reduced TZ‐dSA3‐12's maximal effect by ≈40% (Figure S4f, Supporting Information). These results suggest that TZ‐dSA3‐12 synergistically activates STING through both Fab‐mediated tumor targeting and FcγR‐mediated myeloid engagement. The gene discussed is STING1; the disease is neoplasm.