It was shown JMJD3 was recruited to MIEP upon infection to counteract a suppression of IE gene expression by host intrinsic defense mechanisms, such as those mediated by Daxx protein, while viral UL138 protein is involved to resilience the viral genome by preventing JMJD3’s association with the MIEP.[46] Thus, to confirm these studies and better understand the role of JMJD3 in viral lytic infection, we first conducted a series of JMJD3 siRNA knockdown studies. This evidence concerns the gene KDM6B and infection.