Multiple mechanisms are responsible for the RAAS activation in obesity, including adipose tissue-derived RAAS components that might be involved in regulation of BP and AS through local production of angiotensin (Ang) II and aldosterone, conversion of adipocyte-derived angiotensinogen by systemic renin and ACE-activity, or forming Ang via alternative routes due to the presence of cathepsins and chymase in human adipose tissue [27,30]. This evidence concerns the gene ACE and obesity due to melanocortin 4 receptor deficiency.