KAP1, which coordinates chromatin-remodeling proteins such as Mi2α, SETDB1, and HP1 [257,258,259], recruits the H3K9 methyltransferase, SETDB1, resulting in the deposition of repressive H3K9me3 histone marks at the MIE enhancer/promoter during latent infection [136]. Here, SETDB1 is linked to disease arising from reactivation of latent virus.