This is fully in line with the results reported here and it is tempting to speculate that the infection by EBV, by activating PRMT1 and inactivating PADI4, favours the methylation of the RGG motif of NCL (and possibly of other RGG motif-containing proteins such as EBNA1), thereby increasing their ability to bind to G4 of EBNA1 mRNA, which in turn leads to inhibition of EBNA1 mRNA translation, thus limiting the production of EBNA1-derived antigenic peptides, ultimately leading to immune evasion of EBV. This evidence concerns the gene PRMT1 and infection.