Based on this prediction we suggest that STAT3, BMP2, and IRF1 concordantly regulate NFκB activation upstream in prostate cancer, as it was shown that mechanisms that underline the oncogenic functions of NFκB are likely to require additional transcription factors such as STAT3, which can function cooperatively with NFκB, and are likely to help to drive NFκB-dependent tumorigenesis [7,46]. This evidence concerns the gene IRF1 and Familial prostate cancer.