In microsatellite-stable colorectal cancer, where high miR-21 expression mediates resistance to PD-1 blockade via PTEN suppression and PI3K-AKT–driven PD-L1 upregulation, anti-miR-21 oligonucleotides restore PTEN, reduce PD-L1 levels, and enhance CD8+ T-cell cytotoxicity, achieving a 60% decrease in tumor burden when combined with anti-PD-1 therapy [124]. Here, CD8A is linked to neoplasm.