Deleting the CTCF binding site in EBV LMP1/2 resulted in the disruption of the DNA association between OriP and LMP1/2 loci, an increase in H3K9me3 histone and DNA methylation at the LMP1 promoter region, and severe reduction of EBV latent infection [42]. The gene discussed is PDLIM7; the disease is disease arising from reactivation of latent virus.