Although our previous results showed that knockdown of both STAT2 and IL‐2 almost completely recapitulated the antitumor effects in response to TRIM66 depletion in prostate cancer cells, the predominance of STAT2–IL‐2 in mediating the oncogenic properties of TRIM66 in this disease was yet to be defined. The gene discussed is STAT2; the disease is Familial prostate cancer.