The Epstein-Barr virus (EBV) BNFR1 protein interacts with DAXX to displace ATRX from the complex, effectively reprogramming DAXX and resulting in the activation of early gene transcription (Tsai et al., 2011; Tsai et al., 2014), while degradation of DAXX is promoted by pp71 and E1B-55K during human cytomegalovirus (HCMV), and adenovirus (AdV) infections, respectively (Schreiner et al., 2013; Saffert and Kalejta, 2006). Here, ATRX is linked to infection.