OSCC-derived EVs were shown to promote tumor growth by altering the TME, increasing levels of inflammatory cytokines, including IL-17A, IL-10, IL-1β, and immune checkpoint molecules, including programmed death-ligand 1 (PD-L1), and activating the IL-17A signaling pathway, including TRAF6 and c-FOS. The gene discussed is IL17A; the disease is neoplasm.