A multicenter cross-sectional study showed a solid dose-response relationship between current smoking and higher oral EBV loads [34], smokers were 1.59-fold more likely to have detectable plasma EBV DNA than non-smokers [37], and smoking was reported to increase the NPC risk by repeatedly reactivating EBV [20] with more than 90% of this effect mediated through anti-EBV-VCA-IgA [35]. This evidence concerns the gene CD79A and nasopharyngeal carcinoma.