Therefore, it is reasonable to conclude that EBNA2-dependent transcription of host growth promoting genes, such as c-Myc, initiates oncogene-induced replicative stress and activation of ATM/Chk2-dependent G1/S growth arrest of the majority of infected proliferating cells, while later in infection EBNA2 driven EBNA3C attenuates the expression of oncogenes and inactivates p16 allowing subsequent cellular proliferation despite low, but persistent ATM signaling. Here, CHEK2 is linked to infection.