Given the importance in titrating this potentiallygenotoxic oncoprotein and the known role of ATM in suppressing c-Myc oncogenesis(Hong et al., 2006; Murphy et al., 2008; Pusapati et al., 2006), these findings strongly support amodel of acute oncogenic stress early after EBV infection that is modulatedthrough the well described Wp to Cp switch enabling modest EBNA2 activitycritical for indefinite EBV-infected cell outgrowth. Here, MYC is linked to Epstein-Barr virus infection.