PTEN loss-induced PI3K/Akt has been shown to mediate migration and invasion of prostate cancer cells in response to CXCL12/CXCR4 [20,33,34], suggesting that Akt can function both upstream (as an inducer of CXCR4 expression) and downstream (as a signaling kinase for induction of proteases and invasion) of CXCR4. This evidence concerns the gene CXCR4 and prostate cancer.