The EBV-encoded latent membrane proteins limit the actions of interferon by targeting interferon receptors for degradation, which allows NPC cells to avoid immune surveillance.21 In addition, EBV noncoding RNA molecules enable NPC cells to escape immune recognition by blocking antigen presentation and immune cell activation.22,23 Therefore, a heavy load or an increase in EBV DNA could be associated with more tumor cells escaping immune destruction and result in a poor prognosis and disease progression. The gene discussed is IFNAR2; the disease is neoplasm.