There has been evidence showing that viral infection could interfere with SG formation through various mechanisms (White and Lloyd, 2012), such as inhibiting translational initiation (Linero et al., 2011), sequestering SG components (such as TIA-1, and G3BP1/2) (Nikolic et al., 2016), and interacting with key SG proteins to form stable viral ribonucleoprotein (RNP) complexes (Abrahamyan et al., 2010). The gene discussed is G3BP1; the disease is viral infectious disease.