Our prior work indicates that during the hyper-proliferative burst following EBV infection, cells that succumb to ATM/Chk2-mediated growth arrest have failed to upregulate oxidative phosphorylation and genes associated with mitochondrial biogenesis.38 We hypothesize that this metabolic imbalance may lead to a deficiency in dNTP levels necessary to sustain hyper-proliferation during the first rounds of B-cell division after infection. Here, ATM is linked to infection.