Specifically, knockout of G3BP1/2 in RNase L-null cells, which abolished SG assembly, did not alter RLR-MAVS-IRF3-mediated signaling, induction of interferon β mRNA, or alterations to interferon β protein synthesis in response to dsRNA, 5′-PPP-RNA, or flavivirus infection [59]. The gene discussed is IRF3; the disease is Flavivirus Infections.