In summary, by relying on a universally applicable TME‐responsive mPEG mask, PmTriTNE@CDA rationally integrates multispecific TCE, ICB and STING agonists to transform the cold TME into a hot TME, overcome TNBC heterogeneity by eliminating heterogeneous tumor cells, especially CSCs, and is well tolerated in vivo. The gene discussed is STING1; the disease is neoplasm.