Consistent with this hypothesis, we observed that growth of AR-dependent prostate cancer cells (LNCaP), as well as AR-independent prostate cancer cells (C4-2B, PC-3, DU145, and LNCaP-LN3), was significantly inhibited upon depletion of SETD1A in these cell lines using siRNA or shRNA (Figure 1C–E and Figure S1). This evidence concerns the gene AR and prostate cancer.