Indeed, Testoni et al. pointed out that upon IFN-α treatment in HCC, ISGF3 was recruited to the promoter of DNp73, an antiapoptotic protein and p53 repressor, along with histone deacetylases (HDACs) and EZH2, a component of polycomb repressive complex 2 (PRC2) [162]. This evidence concerns the gene STAT1 and hepatocellular carcinoma.