Resistance to such inhibitory effects may be supported by EBV viral factors: EBERs can avert the blockade of protein synthesis induced by IFNs [128]; LMP2s can enhance turnover in the intracellular pool of IFN-receptors via endosomal-mediated degradation and thus attenuate the inhibitory effects of IFN-γ on NPC cells [129]. The gene discussed is IFNG; the disease is nasopharyngeal carcinoma.