Based on our previous findings detailing that endothelial Kir2.1 channels 1) are critical regulators of endothelial control of vasodilation via NO production (12), and 2) also exhibit a similar profile of dysfunction in obesity [i.e., Kir2.1 is impaired in endothelium of VAT of obese mice and humans but not that of SAT or lean controls (5)], we first aimed to determine if VAT may be a mediator of endothelial Kir2.1 impairment in vitro that may underlie obesity-induced endothelial dysfunction. The gene discussed is KCNJ2; the disease is obesity disorder.