In summary, our results explain (1) how cells maintain the expression of a subset of anti-viral genes despite potent negative feedback mechanisms that quickly downregulate the initial response to IFNβ (Figure 7A) and (2) the mechanism through which DNA damage-resistant cancer cells constitutively upregulate the expression of only the U-ISGF3-dependent subset of ISGs, and not the full set of ISGs including anti-proliferative or pro-apoptotic genes (Figure 7B). This evidence concerns the gene STAT2 and cancer.