Here we found the Cav-1 mediated increases in VEGF-A secretion to be independent of PI3-K/AKT and mTOR signalling, whereas Cav-1 appears to promote both the production and release of VEGF-A [47] in prostate cancer cells at least in part through the potentiation of PI3-K/AKT signalling. This evidence concerns the gene CAV1 and prostate carcinoma.