Given the known involvement of streptolysin in S. iniae virulence [28,30], our results support the hypothesis that the immunoprotectivity of pSagE is probably due at least in part to its ability to induce production of specific serum antibodies, which, upon encountering S. iniae during subsequent infection, may inhibit the function of SagE and thus block S. iniae infection. The gene discussed is SAGE1; the disease is infection.