For example, in many types of viral infection,21–36 viruses neutralize G3BP1 activity and inhibit SG assembly to promote viral replication.37 Various strategies have evolved to accomplish this antagonism, including cleavage of the G3BP1 protein21–27 and/or the production of a protein that directly interacts with a key binding pocket in G3BP1,28–32 thereby inhibiting its ability to drive SG assembly. This evidence concerns the gene G3BP1 and viral infectious disease.