Encouragingly, this CTGF‐LYTAC nanoplatform demonstrated several key capabilities: (i) it enabled tumor‐targeted accumulation and TME‐responsive lysosomal degradation of CTGF; (ii) the depletion of CTGF downregulated the downstream signaling pathways in TNBC cells, disrupted the TNBC/cancer‐associated fibroblasts (CAFs) interactions, and inhibited TNBC growth and metastasis both in vitro and in vivo. This evidence concerns the gene CCN2 and neoplasm.