Latent membrane protein 2A (LMP2A) also induced DNMT1 overexpression via STAT3 activation [88], which led to methylation-silencing of tumor-suppressor gene PTEN. In contrast with epithelial cells, EBV infection of germinal center B cells, the presumptive progenitors of Hodgkin’s lymphoma, down-regulated DNMT1 and DNMT3B via LMP1, whereas DNMT3A was upregulated at the mRNA and protein levels [89]. The gene discussed is DNMT1; the disease is Epstein-Barr virus infection.