Using cultured human prostate cancer cell lines with deficient or insufficient PTEN, not only did we confirm the activation of AKT by KLF5 loss (Figure 6A), we also found that activated AKT indeed mediated the upregulation of HIF1α by KLF5 loss, since treatment with PI3K inhibitors prevented both the activation of AKT and the accumulation of HIF1α (Figure 6C, D). This evidence concerns the gene HIF1A and prostate cancer.