CD274 and neoplasm: These tumours, expressing HPV-16 E5 were resistant to anti-PD-1/PD-L1 immunotherapy, however, use of the antiviral E5 inhibitor, rimantadine, improved the response of this checkpoint blockade immunotherapy, suggesting that HPV-E5 might be evading the T-cell response by abrogating its effector mechanism via PD-L1 expression [350].