The RAS plays a vital role in virtually every cardiovascular disease, and drugs blocking this system are widely used. Three classes can be distinguished, which in essence all block the same renin-ACE-angiotensin II-AT1 receptor pathway. Although for many years it was argued 'the more blockade, the better’, recent trials have shown that this is not the case. In fact, at perhaps slightly more benefit, there are also more side effects. Clearly therefore, we have reached the maximum benefit that can be obtained from blocking this pathway, and we should focus on new RAS components/pathways to interfere with. Indeed, in the last few years multiple new possibilities have emerged: the (pro)renin receptor (which activates renin’s inactive precursor, prorenin), the AT2 receptor (which appears to be stimulated by angiotensin III) and the ACE2-angiotensin-(1-7)-Mas receptor pathway. In addition, angiotensin II stimulates the synthesis and release of aldosterone. Aldosterone receptor antagonists are important tools in resistant hypertension. Simultaneously, new aldosterone receptors emerge, and aldosterone synthase inhibitors are being tested as potential treatment modalities. AT2 receptor (ant)agonists are currently being evaluated clinically, and this is also true for drugs interfering with the ACE2-angiotensin-(1-7)-Mas receptor pathway. Summarizing, the RAS field is rapidly moving "beyond" angiotensin II, and many new drugs start to emerge, including drugs that act on one specific signaling pathway of angiotensin II ("biased AT1 receptor agonists"). The Angiotensin GRC is the only meeting where these topics come together in one meeting. It is THE discussion place for the latest RAS discoveries by investigators from all over the world - all attendants are stimulated to submit an abstract for poster presentation. Combined with a GRS it also attracts a lot of young scientists. Afternoons are saved for informal get-togethers. Discussions usually continue late into the night through convivial gatherings after the evening sessions.