For example, SLX4 was shown to promote Ad5 genome accumulation and protein production [63]; DNA-PK was shown to be activated early during infection with an Ad5 mutant lacking the whole E4 region except E4orf4, and to facilitate E4orf4-induced inactivation of ATM and ATR signaling at the early phase [62]; and ATR activation by Ad12 and hyperphosphorylation of RPA32 were suggested to contribute to inhibition of cellular DNA replication for efficient viral replication, as RPA hyperphosphorylation was reported to inhibit host DNA replication [59]. Here, PRKDC is linked to infection.