Several mechanisms could be used to explain the increase in LVM associated with hyperuricemia, including the systemic inflammatory response, oxidative stress [85, 86], the activity of the renin–angiotensin–aldosterone system [87], endothelial dysfunction [88], and the expression of endothelin-1 in cardiac fibroblasts, which promotes interstitial fibrosis in the myocardium [89]. The gene discussed is EDN1; the disease is endothelial dysfunction.