To determine the predominance of STAT2–IL‐2 signaling in mediating the oncogenic properties of TRIM66 in prostate cancer cells, we performed rescue assay to force overexpressing either STAT2 or IL‐2 in TRIM66‐deficient PC‐3 cells, wherein both manipulations almost completely abolished the inhibitory effects by TRIM66 knockdown on cell proliferation, migration and invasion. This evidence concerns the gene STAT2 and prostate carcinoma.