In MMP-2-rich TME, the anti-PD-L1 peptide can be cleaved from the prodrug PEG-MP9-aPDL1 that accumulated in tumors to impose immune checkpoint blockade, while exposing the stapled peptide MP9 to initiate oncolysis, followed by TAA release and ICD induction, which strengthened tumor infiltration of cytotoxic lymphocytes and resulted in enhanced oncolytic immunotherapy for CRC. This evidence concerns the gene MMP2 and neoplasm.