Proteomic profiling demonstrated that the PLPC exhibits a distinct molecular signature, with a statistically significant over-representation of proteins such as QSOX1, CCL22, FBP2, and SDCBP, each of which has implicated in tumor microenvironment reprogramming, vesicle–immune cell docking, and oxidative-stress-mediated apoptotic signaling [65]. The gene discussed is CCL22; the disease is neoplasm.