Upon entering tumor sites, one end (PD‐L1 ligand) selectively recognizes the mPD‐L1 protein, while the other binds to an E3 ubiquitin ligase or glucagon‐like peptide agonist, thereby hijacking the cellular ubiquitin‐proteasome or lysosomes pathway for mPD‐L1 degradation.[81] Afterward, they can dissociate from the ternary complex for the next degradation cycle. This evidence concerns the gene CD274 and neoplasm.