STAT1 and cancer: Since STAT2 interacted with USP5 after IFN-β treatment and the phosphorylation-deficient STAT2 lost its binding potential (Supplemental Figure 5, F and G), we then knocked out STAT2 in USP5-deficient cancer cells and found that it eliminated the secretion of p-STAT2 and p-STAT1 (Supplemental Figure 5, H and I).