Myriad bacterial anti-phage systems have been described and often the mechanism of programmed cell death is invoked for phage inhibition. However, there is little evidence of "suicide" under physiological conditions for these systems. Instead of death to stop phage propagation, we show here that persister cells are formed and survive using the Escherichia coli C496_10 tripartite toxin/antitoxin system MqsR/MqsA/MqsC that degrades mRNA. Specifically, MqsR/MqsA/MqsC inhibited T2 phage by106-fold and reduced T2 titers by 500-fold. Further evidence of the formation of persister cells during T2 phage attack in the presence of MqsR/MqsA/MqsC include single-cell physiological changes: reduced metabolism (via flow cytometry) and heterogeneous resuscitation. Critically, we found the EcoKI restriction-modification system works in concert with the toxin/antitoxin system to inactivate phage, likely while the cells are in the persister state. Hence, phage attack invokes a stress response similar to that for antibiotics, starvation, and oxidative stress, which leads to persistence, and this dormant state likely allows restriction/modification systems to clear phage DNA.