Loss of Kir2.1 function results in blunted NO production and endothelial dysfunction, and we recently showed that overexpression of Kir2.1 specifically in VAT vascular endothelium was able to restore endothelial function in mesenteric arteries of obese mice via restoring eNOS-mediated NO production (11). The gene discussed is KCNJ2; the disease is endothelial dysfunction.