Moreover, CSCs with high metastatic potential are reportedly located at the leading edge of the tumor.[39] IFN‐β can suppress CSC properties in TNBC.[9a] Thus, we hypothesize that PmTriTNE@CDA efficiently eliminates CSCs by extrinsically targeting CD44‐ and PD‐L1‐high CSCs while intrinsically activating interferon signaling to repress CSCs. The gene discussed is IFNB1; the disease is neoplasm.