Over-activation of CREB was observed in cancer tissues from patients with prostate cancer [38–41], non-small-cell lung cancer [42] and acute leukemia [43], while down-regulation of CREB in several distinct cancer cell lines resulted in inhibition of cell proliferation and induction of apoptosis, suggesting that CREB may be a promising target for cancer therapy [44]. This evidence concerns the gene CREB1 and prostate carcinoma.