Isoflurane exposure to prostate cancer cells promoted HIF-1a and its downstream effector expressions including vascular endothelial growth factor (VEGF), and it increased HIF-1α expression in a concentration- and time-dependent manner; HIF-1α was translocated from the cytoplasm to the nucleus as a transcriptional factor, resulting in promoted proliferation and invasion [13]. This evidence concerns the gene HIF1A and prostate cancer.