HERVs exhibit a paradoxical duality in tumor immunity, functioning both as immunosuppressive mediators and sources of immunogenic neoantigens.The HERVK Env drives immune evasion by upregulating programmed death ligand‐1 (PD‐L1) on tumor and myeloid cells, inducing CD8+ T cell exhaustion—a process amplified by tumor‐derived exosomes that disseminate PD‐L1 as mobile “molecular mines” to systemically suppress T cell activity [125, 142]. Here, ERVW-1 is linked to neoplasm.