Since ATM and Mre11 are known to exert opposing effects on HSV-1 replication in an ICP0-null context, this finding may represent an ability of HSV-1 to kickstart ATM activation early during infection, followed by relocalization of MRN components to the cytoplasm as a means of evading Mre11-dependent suppression at later time points (73). The gene discussed is ATM; the disease is infection.