The most compelling data, in our opinion, supporting the model that the infection-specific activities of HRI are independent of its role as a regulator of protein synthesis is the fact that cells lacking the Ser51 residue of eIF2α (the phosphorylation site of HRI and the other eIF2α kinases) are just as competent as wild-type cells in supporting both the T3S activity of Yersinia as well as the T3S-dependent intracellular proliferation of Chlamydia [4]. This evidence concerns the gene EIF2A and infection.