HIF1α, together with STAT3, has been implicated in transcriptionally regulating VEGF expression via SRC in pancreatic and prostrate carcinomas[71], suppression of HIF1α and STAT3 is associated with anti-angiogenic activity in hypoxic prostate cancer cells[72], and PRL increases VEGF expression in bovine mammary cells[73]. This evidence concerns the gene HIF1A and prostate carcinoma.