EVs from miR-138 -transfected γδ T cell inhibit the proliferation and promote the apoptosis of oral squamous cell carcinoma cells by downregulating GNAI2, FOSL1, CCND1, and CCND3, thereby reducing growth of tumor in xenograft-bearing nude mice; the miR-138-overexpressing EVs also promote the proliferation, interferon-γ secretion and cytotoxicity of CD8+ T cells by downregulating PD-1 and CTLA-4, thereby impairing tumor growth in immunocompetent C3H mice [157]. The gene discussed is CCND1; the disease is neoplasm.