The possible mechanisms underlying the observed reduction of cancer-specific death risk following the ARB and ACE inhibitors medication use include reduction of inflammation, tumour angiogenesis, invasion and peritoneal dissemination in human ovarian cancer cells by blockage of angiotensin receptors (both Angiotensin II type 1 receptor (AT1R) and Angiotensin II type 2 receptor (AT2R)) [6, 12]. This evidence concerns the gene ACE and ovarian carcinoma.