SOAT1 and viral infectious disease: Furthermore, CRISPR-induced knockout of signal transducer and activator of transcription factor 1 (STAT1) in the background of STAG2 deficiency completely abolished ISG expression and these double knockout cells re-gained their susceptibility to RV and VSV infections to levels comparable to WT HT-29 cells (Fig. 2e and Supplementary Fig. 4F), supporting the conclusion that a hyperactive IFN-JAK-STAT pathway is responsible for suppressing multiple viral infections in STAG2−/− cells.