Since the strong host RNAP-dependent early gene promoters T7 A1-A3 are the only target for the host RNAP following host chromosome degradation by Gp3 and Gp6 (which would further explain the weak affinity of Gp5.7 to DNA as it does not have to compete for DNA sites), our results indicate that Gp5.7 could provide another layer of control to specifically counteract the host RNAP activity at T7 A1-A3 that has escaped inhibition of Gp2 at this point in the infection cycle to ensure optimal infection outcome. This evidence concerns the gene GP2 and infection.