For example, 17-DMAG binds to HSP90 and inhibits its function, which eventually results in the degradation of HSP90 client proteins 45; KU675, a novel C-terminal HSP90 inhibitor, has potent anti-proliferative and cytotoxic activity along with client protein degradation, without the induction of a heat-shock response in both androgen-dependent and -independent prostate cancer cell lines 46; and triptolide inhibits HSP90β in a three-fold manner to decrease the CDK4 protein levels in HeLa cells, causing a reduction in the phosphorylation of Rb, and resulting in cell-cycle-arrest at G1 47. This evidence concerns the gene RB1 and prostate cancer.