A possible hypothesis is that the increased EAT volume, influenced by both genetic and environmental factors, leads to heightened production of vasoactive peptides and pro-inflammatory mediators.42 This process could activate the renin-angiotensin system and launch an inflammatory environment, pathophysiological mechanisms could lead to an elevation of arterial blood pressure, and potentially contribute to early onset atherosclerosis. This evidence concerns the gene REN and atherosclerosis.